Title of Invention: Glycoside compound and preparation method therefor, composition, application, and intermediate Abstract: The present invention discloses a glycoside compound represented by Formula III, and a preparation method, a composition, use and an intermediate thereof. The glycoside compound provided in the present invention has simple preparation method, can significantly increase the expression of VEGF-A mRNA, and is effective in promoting the angiogenesis. This provides a reliable guarantee for the development of drugs with pro-angiogenic activity for treating cerebral infarction cerebral stroke, myocardial infarction, and ischemic microcirculatory disturbance of lower limbs. Detailed Description: Part general_description_paragraphs: Part BACKGROUND: Part Technical Field: The present invention relates to a glycoside compound, and a preparation method, a composition, use and an intermediate thereof. Part Related Art: In recent years, research on drugs directed against angiogenesis has attracted more and more attention, and angiogenesis has become a potential biological target for drug intervention in the treatment of cancers, vascular diseases and chronic inflammation. The development of drugs, such as anti-angiogenesis inhibitors intended to reduce tumor angiogenesis, has become a successful way for treatment of many advanced and aggressive cancers. The discovery of pro-angiogenesis has provided a new direction for the effective treatment of ischemic vascular diseases, and it has also become a research hotspot in the medical field. By means of pro-angiogenesis, it is expected to ameliorate major diseases that endanger human health, for example, cardio-cerebrovascular diseases (such as angina pectoris, myocardial infarction, cerebral infarction, and stroke) and lower limb ischemia (such as diabetic lower limb vascular diseases, and thromboangiitis obliterans) caused by microcirculatory disturbance. Cerebrovascular diseases refer to a group of diseases in which pathological changes occur to cerebral arteries or carotid arteries that dominate the brain, causing the intracranial blood circulation disturbance and damage to brain tissue. Clinically, the main manifestations are sudden fainting, unconsciousness, or accompanying deviated mouth and eyes, slurring of speech, and hemiparalysis. Ischemic cerebrovascular diseases mainly refer to cerebral thrombosis, cerebral embolism, and multiple cerebral infarction, etc. The diseases are characterized by sudden attack, rapid progress, and critical condition. Because the diseases are often found in the elderly and tend to be complicated by multiple organ damage, the prognosis is poor and the mortality rate is high. Ischemic cerebrovascular diseases are known as cerebral infarction due to ischemic necrosis of the brain tissue in a corresponding area resulting from sharp interruption of blood flow in the cerebral arteries. Cerebral stroke, also known as “stroke” and cerebralvascular accident (CVA), is one of the most notorious fatal diseases in the world. It is a group of diseases where brain tissue damage is caused by the sudden rupture of blood vessels in the brain or the failure of blood to flow to the brain due to blocked blood vessels, and includes ischemic and hemorrhagic stroke. The incidence of ischemic stroke is higher than that of hemorrhagic stroke. Ischemic stroke is ischemic-hypoxic injury and necrosis of the brain tissue caused by blood supply disorders in local brain tissue region due to a variety of causes, which in turn leads to such clinical manifestations as corresponding neurologic deficits, and severely affects the quality of life of patients. The research focus on pathological intervention of ischemic injury is mainly to improve the cerebral blood circulation and neuroprotection. Among them, the measure to improve cerebral blood circulation is mainly antithrombotic icruz@example.net. Antithrombotic drugs include thrombolytic drugs, platelet aggregation inhibitors and anticoagulants. Existing neuroprotective drugs mainly include calcium antagonists, glutamate antagonists, glutamate release inhibitors, GABA receptor agonists, free radical scavengers, cell membrane stabilizers, and others. The discovery of pro-angiogenesis in recent years has provided a new direction for the effective treatment of ischemic vascular diseases, and it has also become a research hotspot in the medical field. Angiogenesis can promote the neuron survival after cerebral stroke, and improve the neurological deficits and quality of life of the patients after stroke. However, the influencing factors and regulatory mechanisms of angiogenesis after cerebral stroke are complicated. Recent studies have found that PAR1 is involved in microangiogenesis and nerve repair after stroke. Angiogenesis refers to the formation of new capillaries by germination and/or non-germination on the basis of original blood vessels. Angiogenesis mainly includes the process of increase of vascular permeability; production of proteolytic enzymes to degrade the extracellular matrix, and promote endothelial cell proliferation; detachment of endothelial cells from the basement membrane and migration to the Virchow-Robin space to form a three-dimensional lumen through adhesion, proliferation, and reconstruction; differentiation into new capillaries; and interstitial cells entering the vessel wall as induced by an intermediary molecule, to make the blood vessels stable and mature. Under normal physiological conditions, once the blood vessels are formed in the body, they remain highly stable, and are regulated by many key molecules that have positive or negative regulatory effects (that is, pro-angiogenic and anti-angiogenic factors). The initiation of angiogenesis is only turned on briefly with the appearance of the stimulus signal, and then turned off, to maintain a dynamic balance between angiogenesis and decline. Factors affecting microangiogenesis after cerebral stroke include: local blood and oxygen supply; changes in thrombin and its concentration; and levels of pro-angiogenic factors, such as hypoxia-inducible factor 1a (HIF-1a), vascular endothelial growth factor (VEGF), matrix metalloproteinases (MMPs), angiopoietin 1 (Ang-1), and angiopoietin 2 (Ang-2), etc. PAR1 usually interacts with pro-angiogenic factors and plays a role in promoting angiogenesis. VEGF is currently recognized as a factor that plays a key role in angiogenesis. Normally, VEGF is expressed only at a low level to maintain the blood vessel density and permeability under physiological conditions. Some pathological processes such as inflammation, tumors, wound healing, ischemia, and hypoxia can promote the VEGF expression. In patients with cerebral stroke, neurons and glial cells around the focus have increased expression of VEGF. By specifically binding to cell surface receptors on endothelial cells, VEGF can promote the proliferation and migration of vascular endothelial cells, increase the vascular permeability, and enhance the expression of factors that degrade extracellular matrix, thereby promoting microangiogenesis. However, drugs with clear therapeutic angiogenesis are still in the stage of transition from laboratory to clinical trial. For example, the product Generx available from Cardium Therapeutics is an angiogenic FGF4 gene therapy for the treatment of myocardial microvascular dysfunction. It is currently in the phase III clinical trial. Therefore, how to find a simple, stable and effective drug with pro-angiogenic activity is a research hotspot and challenge for those skilled in the art. Part SUMMARY: To solve the technical problem in the prior art that drugs with clear therapeutic angiogenesis are not available in the market and the preparation of drugs is difficult, the present invention provides a glycoside compound, and a preparation method, a composition, use and an intermediate thereof. The glycoside compound provided in the present invention has simple preparation method, can significantly increase the expression of VEGF-A mRNA, and is useful in the preparation of pro-angiogenic drugs. This provides a reliable guarantee for the development of drugs with pro-angiogenic activity for treating ischemic cardio-cerebrovascular diseases, particularly cerebral infarction (cerebral stroke), myocardial infarction, and ischemic microcirculatory disturbance of lower limbs. The above technical problems are solved in the present invention through the following technical solutions. The present invention provides a glycoside compound represented by Formula III below, or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof: in which R1, R2, R1, R4 and R5 are each independently selected from the group consisting of hydrogen, hydroxyl, mercapto, a substituted or unsubstituted C1-C20 alkoxy group, nitro or halo; or any adjacent two of R1, R2, R3, R4 and R5 form, together with carbon atoms on the phenyl ring to which they are attached, a 5- to 7-membered heterocyclic ring having a heteroatom that is O or S, where one or more heteroatoms may be present, and when more than one heteroatoms are present, the heteroatoms may be the same or different, where the substituent in the substituted or unsubstituted C1-C20 alkoxy group is selected from the group consisting of a C3-C20 cycloalkyl group, a C1-C20 alkenyl group, a substituted or unsubstituted C6-C20 aryl group, halo, a substituted or unsubstituted C2-C20 heteroaryl group, a C3-C6 cycloalkoxy group, a C1-C20 alkoxy group, or a C1-C20 alkyl group, in which the substituent in the substituted or unsubstituted C6-C20 aryl group and the substituted or unsubstituted C2-C20 heteroaryl group is each independently halo or a halo-substituted C1-C20 alkyl group; X is CH2, NR7, O or S; Y is CH2, NR8, O or S; Z is O or S; R1 and R8 are each independently hydrogen, an aryl-substituted C1-C6 alkoxycarbonyl group, or a C1-C6 alkoxycarbonyl group; each R6 is independently hydrogen or glycosyl; and n is 2, 3 or 4. Preferably: when X is CH2, Y is CH2, and n=2, 3 or 4, R1-R5 are not all H; when n=2, R1, R4 and R5 are H, R2 and R3 are not both OCH; and OH; when n=2, R1, R2 and R5 are H, R3 and R5 are not both OH and OCH3; when n=2, R2, R4 and R5 are H, R1 and R3 are not both OH; and when n=2, R1, R2 and R4 are H, R3 and R5 are not both OH. The present invention provides a glycoside compound represented by Formula I below, or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof: R1, R2, R3, R4 and R5 are each independently selected from the group consisting of hydrogen, hydroxyl, mercapto, a substituted or unsubstituted C1-C20 alkoxy group (for example, a substituted or unsubstituted C1-C10 alkoxy group, such as a substituted or unsubstituted C1-C6 alkoxy group), nitro, or halo; or any adjacent two of R1, R2, R3, R4 and R5 form, together with carbon atoms on the phenyl ring to which they are attached, a 5- to 7-membered heterocyclic ring (for example, R2 and R3 form a 5- to 7-membered heterocyclic ring) having a heteroatom that is O or S (for example, O), where one or more (for example, two) heteroatoms may be present, and when more than one heteroatoms are present, the heteroatoms may be the same or different, in which the substituent in the substituted or unsubstituted C1-C20 alkoxy group is selected from the group consisting of a C3-C20 cycloalkyl group (for example, a C3-C10 cycloalkyl group, such as a C3-C6 cycloalkyl group), a C2-C20 alkenyl group (for example, a C2-C6 alkenyl, such as a C2-C4 alkenyl, for example a substituted or unsubstituted C6-C20 aryl group (for example, a substituted or unsubstituted C6-C10 aryl group, such as substituted or unsubstituted aryl or naphthyl), halo (for example, fluoro, chloro, bromo or iodo), a substituted or unsubstituted C2-C20 heteroaryl group in which the heteroatom is one or more selected from the group consisting of N, S and O (for example, 1 heteroatom is present; for example, the heteroatom is N; for example, the substituted or unsubstituted C2-C20 heteroaryl group is a monocyclic heteroaryl group). (for example, a substituted or unsubstituted C2-C10 heteroaryl group, such as a substituted or unsubstituted C2-C6 heteroaryl group), a C3-C6 cycloalkoxy group (e.g. a C1-C20 alkoxy group (for example, a C1-C10 alkoxy group, such as a C1-C6 alkoxy group, for example, methoxy, ethoxy or propoxy) or a C1-C20 alkyl group (for example, a C1-C10 alkyl group, such as a C1-C6 alkyl group, for example a C1-C3 alkyl group), where the substituent in the substituted or unsubstituted C1-C20 aryl group and the substituted or unsubstituted C2-C20 heteroaryl group is each independently selected from halo (for example, fluoro, chloro, bromo or iodo) or a halo (for example, fluoro, chloro, bromo or iodo)-substituted C1-C20 alkyl group (where one or more substituents may be present in the halo-substituted C1-C20 alkyl group, and when more than one heteroatoms are present, the heteroatoms may be the same or different; for example, a halo-substituted C1-C10 alkyl group, for example, a halo-substituted C1-C6 alkyl group, for example, a halo-substituted C1-C3 alkyl group, for example, —CF3, —CHF2 or —CH2F); X is CH2, NR7, O or S; Y is CH2, NR8, O or S; Z is O or S; R7 and R8 are each independently hydrogen, an aryl-substituted C1-C6 alkoxycarbonyl group (e.g. benzoxycarbonyl) or a C1-C6 alkoxycarbonyl group (e.g. tert-butoxycarbonyl); R6 is hydrogen or and n is 2, 3 or 4. Preferably: when X is CH2, Y is CH2, and n=2, 3 or 4, R1-R5 are not all H; when n=2, R1, R4 and R5 are H, R2 and R3 are not both OCH3 and OH; and when n=2, R1, R2 and R5 are H, R3 and R4 are not both OH and OCH3. In the present invention, the substituted or unsubstituted C2-C20 heteroaryl group may be substituted or unsubstituted pyrrolyl, substituted or unsubstituted furyl, substituted or unsubstituted thienyl, substituted or unsubstituted pyrazolyl, substituted or unsubstituted imidazolyl, substituted or unsubstituted oxazolyl, substituted or unsubstituted thiazolyl, substituted or unsubstituted isoxazolyl, substituted or unsubstituted pyridinyl, substituted or unsubstituted pyridazinyl, substituted or unsubstituted pyrimidinyl, or substituted or unsubstituted pyrazinyl, for example, substituted or unsubstituted pyridinyl. In the present invention, the unsubstituted C1-C20 alkoxy group may be In the present invention, the C3-C20 cycloalkyl group may be cyclopropyl, cyclobutyl, cyclopentyl or cyclohexyl. In the present invention, the substituted C6-C20 aryl group may be In the present invention, the substituted C1-C20 alkoxy group may be In the present invention, the unsubstituted C2-C20 heteroaryl group may be In the present invention, the 5- to 7-membered heterocyclic ring may be In the present invention, R1 may be hydrogen. In the present invention, R2 may be hydrogen, or a substituted or unsubstituted C1-C20 alkoxy group, or R2 and R3 form where the substituted or unsubstituted C1-C20 alkoxy group and substituents thereof are as defined above. In the present invention, R3 may be hydrogen, hydroxyl, mercapto, a substituted or unsubstituted C1-C20 alkoxy group, hydroxyl, nitro or halo, where the substituted or unsubstituted C1-C20 alkoxy group and substituents thereof, and halo are as defined above. In the present invention, R4 may be hydrogen, or a substituted or unsubstituted C1-C20 alkoxy group, where the substituted or unsubstituted C1-C20 alkoxy group and substituents thereof are as defined above. In the present invention, R5 may be hydrogen. In an embodiment of the present invention, the definitions of various groups are as follows (the definitions of the unmentioned groups are as described above). X is CH2; and Y is CH2, NR8, S or O, in which RA is hydrogen, an aryl-substituted alkoxycarbonyl group or an alkoxycarbonyl group. In an embodiment of the present invention, the definitions of various groups are as follows (the definitions of the unmentioned groups are as described above). X is NR7; and Y is CH2, in which R7 is hydrogen, an aryl-substituted alkoxycarbonyl group, or an alkoxycarbonylgroup. In an embodiment of the present invention, the definitions of various groups are as follows (the definitions of the unmentioned groups are as described above). X is O or S; and Y is CH2. In the present invention, when R1, R2, R3, R4 and R5 are each independently selected from hydrogen, hydroxyl, mercapto, a substituted or unsubstituted C1-C20 alkoxy group, nitro or halo, one or more (for example, 1, 2, or 3, such as 1) substituted or unsubstituted C1-C20 alkoxy groups may be present. In the present invention, may have any of the following structures: In the present invention, preferably, n=2. In the present invention, preferably, R1, R2, R3, R4 and R5 are each independently selected from hydrogen, a substituted or unsubstituted C1-C20 alkoxy group, nitro or halo. In the present invention, preferably, R6 is hydrogen. In the present invention, preferably, the optical isomer of in the compound represented by Formula I may be: and further preferably In a certain embodiment of the present invention, the substituents in the compound of Formula I may be the following (the definitions of the unmentioned groups are as described above): n is 2, 3 or 4; and X is CH2, NR7, O or S. In a certain embodiment of the present invention, the substituents in the compound of Formula I may be the following (the definitions of the unmentioned groups are as described above): n is 2, 3 or 4; and Y is CH2, NR, O or S. In a certain embodiment of the present invention, the substituents in the compound of Formula I may be the following (the definitions of the unmentioned groups are as described above): R1 is hydrogen; R2 is hydrogen, or a substituted or unsubstituted C1-C20 alkoxy group, or R2 and W form where the substituted or unsubstituted C1-C20 alkoxy group and substituents thereof are as defined above; R3 is hydrogen, hydroxyl, mercapto, a substituted or unsubstituted C1-C20 alkoxy group, hydroxyl, nitro or halo, where the substituted or unsubstituted C1-C20 alkoxy group and substituents thereof, and halo are as defined above; R4 is hydrogen, or a substituted or unsubstituted C1-C20 alkoxy group, where the substituted or unsubstituted C1-C20 alkoxy group and substituents thereof are as defined above; and R5 is hydrogen. In a certain embodiment of the present invention, the substituents in the compound of Formula I may be the following (the definitions of the unmentioned groups are as described above): n is 2; when X is CH2, Y is CH2, NR3, S or O; when X is NR7, Y is CH2; and when X is O or S, Y is CH2. The present invention also provides compounds of any of the following structures: Preferably, these compounds are: The present invention also provides a method for preparing a glycoside compound, which comprises the steps of reducing a compound represented by Formula V in a solvent to obtain a compound represented by Formula VI: where R9′, R10′ and R11′ are each independently hydrogen or Ac, and at least one of them is Ac; R6 is hydrogen, Ac or R12′, R13′, R14′, and R15′ are each independently hydrogen, Bz or Ac; n, X, Y, Z, R1, R2, R3, R4, R5 and R6 are as defined above; when R6′ is hydrogen or Ac, R6 is hydrogen; and when R6′ is R6 is OH The present invention also provides a method for preparing a compound represented by Formula I, which comprises the steps of: reducing a compound represented by Formula II in a solvent to obtain the compound represented by Formula I: where R9′, R10′ and R11′ are each independently hydrogen or Ac, and at least one of them is Ac; R6 is hydrogen, Ac or R12′, R13′, R14′, and R15′ are each independently hydrogen, Bz or Ac; n, X, Y, Z, R1, R2, R3, R4, R5 and R6 are as defined above; when R6′ is hydrogen or Ac, R6 is hydrogen; and when R6′ is R6 is OH The present invention also provides use of the glycoside compound, or a compound below, or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof, in the preparation of pro-angiogenic drugs: The present invention also provides use of the glycoside compound represented by Formula I, Compound TG-052, Compound TG-053, Compound TG-054 or TG-057, or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof, in the preparation of pro-angiogenic drugs: The present invention also provides use of the glycoside compound, or a compound below, or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof, in the preparation of drugs for treating ischemic cardio-cerebrovascular diseases, particularly cerebral infarction (cerebral stroke) and myocardial infarction, and ischemic microcirculatory disturbance of lower limbs: The present invention also provides use of the glycoside compound represented by Formula I, Compound TG-052, Compound TG-053, or Compound TG-054, or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof, in the preparation of drugs for treating ischemic cardio-cerebrovascular diseases, particularly cerebral infarction (cerebral stroke) and myocardial infarction, and ischemic microcirculatory disturbance of lower limbs: The ischemic cardio-cerebrovascular diseases involve vascular wall lesions, and all symptoms and/or pathological changes in the early to late stages of tissue ischemia of heart and brain, such as cerebral infarction (cerebral stroke) or myocardial infarction, caused by vascular lesions due to changes in blood composition and/or hemodynamic changes. The present invention also provides an intermediate of the glycoside compound shown above: The present invention also provides an intermediate of the glycoside compound represented by Formula I: The present invention further provides use of the glycoside compound, or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof, in pro-angiogenic drugs for the prevention and/or treatment of preferably ischemic vascular diseases, and further preferably ischemic cardio-cerebrovascular diseases, particularly cerebral infarction (cerebral stroke) and myocardial infarction, and ischemic microcirculatory disturbance of lower limbs. In one aspect, this can be implemented as use of the glycoside compound, or a compound below, or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof, in the preparation of drugs that are used to prevent and/or treat ischemic vascular diseases in mammals, including humans, by promoting angiogenesis. They are further preferably used in ischemic cardio-cerebrovascular diseases, particularly cerebral infarction (cerebral stroke), myocardial infarction, and ischemic diseases of lower limbs. In another aspect, this can be implemented as a method for promoting angiogenesis in a patient in need thereof, preferably a method for treating and/or preventing a mammal (including human) having or susceptible to ischemic vascular disease, and further preferably a method for treating and/or preventing a mammal (including human) having or susceptible to ischemic cardio-cerebrovascular diseases, particularly cerebral infarction (cerebral stroke), myocardial infarction, and ischemic microcirculatory disturbance of lower limbs. The method comprises administering, to the patient, a therapeutically effective amount of the glycoside compound of the present invention, or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof, together with a pharmaceutically acceptable excipient or carrier. Further, use of the glycoside compound of the present invention, or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof, in the prevention and/or treatment of ischemic vascular diseases is provided. Examples of ischemic cerebrovascular diseases include cerebral stroke, atherosclerotic cerebral thrombosis, cardiogenic cerebral embolism, acute ischemic cerebrovascular syndrome, small vessel disease (also known as lacunar stroke), multiple cerebral infarction, massive cerebral infarction, cerebral watershed infarction, hemorrhagic infarction, asymptomatic cerebral infarction, cerebral venous and cerebral venous sinus thrombosis, Moyamoya disease, and ischemic cerebral stroke due to other causes. In a preferred embodiment, the ischemic cerebrovascular disease is atherosclerotic cerebral thrombosis, which is occlusion of the lumen caused by thrombus formed on the basis of atherosclerosis and various vascular diseases such as arteritis, causing clinical syndromes such as ischemia, hypoxia, necrosis, and softening of brain tissues. In another preferred embodiment, the ischemic cerebrovascular disease is cardiogenic cerebral embolism, which is cerebral infarction caused by vascular occlusion due to the distal migration of cardiogenic emboli to the cerebral artery system through the blood flow path. In another preferred embodiment, the ischemic cerebrovascular disease is acute ischemic cerebrovascular syndrome, which includes transient ischemic attack, reversible ischemic neurological deficit and cerebral stroke with full recovery. In another preferred embodiment, the cerebrovascular disease is cerebral stroke. It is a group of diseases where brain tissue damage is caused by the sudden rupture of blood vessels in the brain or the failure of blood to flow to the brain due to blocked blood vessels, and includes ischemic and hemorrhagic stroke. Preferably, a therapeutically effective amount of the glycoside compound of the present invention, or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof is administered to a patient in need thereof through a common route of administration in a conventional pharmaceutical composition (comprising an effective amount of the active ingredient and a suitable pharmaceutical carrier) and dosage form formulated for administration according to methods known in the art. A “therapeutically effective amount” refers to an amount of the active ingredient which, when administered, is sufficient to prevent the development of, or to a certain extent alleviate one or more symptoms of the disease of interest. The specific dose of the compound administered according to the present invention is determined by the specific conditions of the case, including the compound administered, the route of administration, the specific status being treated, and similar considerations. In particular, a “therapeutically effective amount of a compound” refers to an amount of a compound sufficient to prevent or to some extent alleviate one or more ischemic vascular diseases. The ischemic vascular diseases are particularly cerebral infarction (cerebral stroke), myocardial infarction, and ischemic diseases of the lower limbs, etc. Further, the ischemic cerebrovascular diseases include cerebral stroke, atherosclerotic cerebral thrombosis, cardiogenic cerebral embolism, acute ischemic cerebrovascular syndrome, small vessel disease (also known as lacunar stroke), multiple cerebral infarction, massive cerebral infarction, cerebral watershed infarction, hemorrhagic infarction, asymptomatic cerebral infarction, cerebral venous and cerebral venous sinus thrombosis, Moyamoya disease, and ischemic cerebral stroke due to other causes. Depending on the type and severity of the ischemic vascular disease to be treated and the response of specific patient to the drug treatment, the single dose and daily dose are different. Therefore, an accurate single dose will be determined based on standard medical principles under the guidance of a doctor. An effective daily dose of the glycoside compound according to the present invention of 0.01 mg to about 1000 mg, about 1 mg to about 500 mg, or about 10 mg to about 200 mg, and optionally about 0.01 mg to about 2000 mg, about 10 mg to about 1000 mg, about 100 mg to about 800 mg, or about 200 mg to about 600 mg of an additional active agent in an oral dosage form are used in the treatment of ischemic vascular diseases. The glycoside compound of the present invention, or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof may be used alone or in combination, or in a combined therapy with other therapeutic agents. In an embodiment of the present invention, the glycoside compound, or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof, is used in the prevention and/or treatment of ischemic vascular diseases, where the prevention or treatment includes administration to use as a sole active ingredient. In another embodiment of the present invention, the glycoside compound, or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof, is used in the prevention and/or treatment of ischemic vascular diseases, where the prevention or treatment includes administration in a combined therapy with a therapeutic agent selected from the group consisting of another glycoside compound or the present invention or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof, antihypertensive drugs, lipid-lowering drugs, thrombolytic drugs, platelet aggregation inhibitors, anticoagulants, neuroprotective drugs, calcium antagonists, glutamate antagonists, glutamate release inhibitors, GABA receptor agonists, free radical scavengers, and cell membrane stabilizers. In a preferred embodiment of the present invention, the additional therapeutic agent is selected from the group consisting of another glycoside compound of the present invention or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof, Reteplase, Lanoteplase, Monteplase, Douchi Fibrinolytic Enzyme, new earthworm fibrinolytic enzyme, Nattokinase, snake venom plasminogen activator, Aspirin, Ticlopidine, Clopidogrel, Prasugrel, Ticagrelor, Cangrelor, sarpogrelate hydrochloride, vorapaxar, atopaxar, heparin, low molecular weight heparin, warfarin, Rivaroxaban, Bivalirudin, Pradaxa, Edaravone, and Statins. As will be apparent to those skilled in the art, a combination of the present invention comprising a glycoside compound of the present invention or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof and an additional therapeutic agent is effective not only when these active ingredients are used in a single composition, but also when they are used in two different compositions (administered simultaneously, sequentially or separately after a period of time). In addition, it will be appreciated by those skilled in the art that the glycoside compound of the present invention or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof, can be prescribed to use in a combined therapy with an additional active ingredients, to prevent and/or treat ischemic vascular diseases. In a particular embodiment, the combined therapy comprises simultaneously, sequentially or separately administering the glycoside compound of the present invention or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof, and the additional therapeutic agent, to a subject. Alternatively, the combined therapy comprises administering the glycoside compound of the invention or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof, and an additional therapeutic agent in a single composition, to a subject. In an embodiment of the present invention, the glycoside compound of the present invention or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof can be conveniently administered to a patient. Therefore, the compound used for the purpose of the present invention can be in the form of a pharmaceutical composition comprising an effective amount of the glycoside compound of the present invention or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof in combination with a pharmaceutically acceptable excipient or carrier. This aspect can also be implemented as a composition comprising an effective amount of the glycoside compound of the present invention or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof in combination with a pharmaceutically acceptable excipient or carrier, which is used in the prevention and/or treatment of cerebral infarction, cerebral stroke, atherosclerotic cerebral thrombosis, cardiogenic cerebral embolism, acute ischemic cerebrovascular syndrome, small vessel disease (also known as lacunar stroke), multiple cerebral infarction, massive cerebral infarction, cerebral watershed infarction, hemorrhagic infarction, asymptomatic cerebral infarction, cerebral venous and cerebral venous sinus thrombosis, Moyamoya disease, and ischemic cerebral stroke due to other causes. In one embodiment of the present invention, the compound used can be administered in the form of a unit dosage preparation comprising a pharmaceutically acceptable conventional carrier through a route of administration including oral, injection, subcutaneous, intratracheal, transdermal, parenteral, rectal, topical, intravenous, and intramuscular administration, or others. The pharmaceutical composition can be formulated into any medicinal form, such as tablets, granules, injections, gels, pills, capsules, suppositories, implants, nano-preparations, and powder injections. Some dosage forms such as tablets and capsules can be subdivided into suitable unit dosage forms comprising an appropriate amount of the active ingredient, such as an effective amount to achieve the desired purpose. In another embodiment, the glycoside compound of the present invention used for the purpose of the present invention, or a tautomer, an optical isomer, a solvate, a polymorph, a pharmaceutically acceptable salt or ester, or a pharmaceutically acceptable prodrug or derivative thereof is in an injectable preparation to be administered to a patient to be treated. Suitable injectable preparations in the present invention include a sterilized or sterile solution, emulsion or suspension made of a drug and a suitable solvent or dispersion medium for injection into a human, and a sterile powder preparation for being formulated into a solution or suspension before use. The injectable preparation includes an injectable solution (where a large-volume injectable solution for intravenous drip is also known as an intravenous infusion), a sterile powder for injection and a concentrated solution for injection. The carrier includes excipients and diluents, which need to have a sufficiently high purity and a very low toxicity to make them suitable for being administered to a patient to be treated. The carrier can be inert or have pharmaceutical benefits itself. The types of carriers include, but are not limited to, diluents such as fillers and bulking agents, binders, lubricants, anti-caking agents, disintegrants, sweeteners, buffers, preservatives, solubilizers, isotonic agents, suspending agents and dispersants, wetting or emulsifying agents, flavoring and fragrances, thickeners, and vehicles. Some carriers can be listed in more than one category, for example, vegetable oils can be used as a lubricant in some preparations and as a diluent in other preparations. Exemplary pharmaceutically acceptable carriers include sugar, starch, cellulose, malt, gelatin, talc and vegetable oils. Optional active agents can be contained in the pharmaceutical composition, which do not substantially affect the activity of the compound of the present invention. The present invention has the following positive effects. The glycoside compound provided in the present invention has simple preparation method, can significantly increase the expression of VEGF-A mRNA, and is useful in the preparation of pro-angiogenic drugs. This provides a reliable guarantee for the development of drugs with pro-angiogenic activity for treating cerebral infarction cerebral stroke, myocardial infarction, and ischemic microcirculatory disturbance of lower limbs. The compound or its salt of the present application may be the sole active agent administered or may be administered in conjunction with other active agents. Part Definition of Terms: “Stereoisomers”, “optical isomers” or “optically active isomers” are compounds that have the same chemical composition but different arrangements of atoms or groups in space. They include “diastereomers” and “enantiomers”. “Diastereomers” are stereoisomers that have two or more centers of chirality and whose molecules are not mirror images of each other. Diastereomers have different physical properties, such as melting point, boiling point, spectral characteristics and reactivity. In the presence of a resolving agent or chromatography, a mixture of diastereomers can be separated by a high-resolution analytical step such as electrophoresis and crystallization using, for example, a chiral HPLC column. “Enantiomers” refer to two stereoisomers of a compound that are not overlapping mirror images of each other. A 50:50 mixture of enantiomers is called a racemic mixture or a racemate, which may occur during a chemical reaction or a treatment process when no stereoselectivity or stereospecificity is available. “Alkyl” includes both branched and linear saturated aliphatic hydrocarbon groups, and has a specified number of carbon atoms, typically 1 to about 12 carbon atoms. The term C1-C6 alkyl group as used herein means an alkyl group having 1 to about 6 carbon atoms. When the C0-Cn alkyl group is used herein in combination with another group, for example, (phenyl)C0-C4 alkyl, in this specified group, phenyl is directly bonded through a single covalent bond (C0) or connected via an alkyl group with a specified number of carbon atoms (in this case, 1 to about 4 carbon atoms). Examples of the alkyl group include, but are not limited to: methyl, ethyl, n-propyl, isopropyl, n-butyl, 3-methylbutyl, tert-butyl, n-pentyl, and sec-pentyl. “Alkenyl” refers to linear and branched hydrocarbon groups including one or more unsaturated carbon-carbon double bonds. The carbon-carbon double bonds may be present at any stable point along the chain. The alkenyl groups described herein typically have 2 to about 12 carbon atoms. Preferred alkenyl groups are lower alkenyl groups, having 2 to about 8 carbon atoms, for example, C2-C8, C2-C6, and C2-C4 alkenyl groups. Examples of alkenyl groups include ethenyl, propenyl, and butenyl. “Alkoxy” refers to an alkyl group, as defined above, having a specified number of carbon atoms and connected via an oxygen bridge. Examples of alkoxy groups include, but are not limited to, methoxy, ethoxy, 3-hexyloxy, and 3-methylpentyloxy. The term “heterocycle” means a 5- to 8-membered saturated ring, partially unsaturated ring, or aromatic ring containing 1 to about 4 heteroatoms selected from N, O, and S, with the remaining ring atoms being carbon; or a 7- to 11-membered saturated ring, partially unsaturated ring, or aromatic heterocyclic ring system, and a 10- to 15-membered tricyclic ring system, where the system contains at least 1 heteroatom selected from N, O and S in the polycyclic ring system and containing up to about 4 heteroatoms independently selected from N, O and S in each ring of the polycyclic ring system. Unless otherwise specified, a heterocycle may be attached to a group that is amenable to substitution and produces a stable structure at any heteroatom and carbon atom of the heterocycle. As indicated, the heterocycle described herein may be substituted on a carbon or nitrogen atom, provided that the resulting compound is stable. The nitrogen atom in a heterocyclic ring may optionally be quaternized. It is preferred that the total number of heteroatoms in the heterocyclyl group is not more than 4 and that the total number of S and O atoms in the heterocyclyl group is not more than 2, and more preferably not more than 1. Examples of heterocyclyl groups include pyridinyl, indolyl, pyrimidinyl, pyridizinyl, pyrazinyl, imidazolyl, oxazolyl, furyl, phenylthio, thiazolyl, triazolyl, tetrazolyl, isoxazolyl, quinolinyl, pyrrolyl, pyrazolyl, benz[b]thiophenyl, isoquinolinyl, quinazolinyl, quinoxalinyl, thienyl, isoindolyl, dihydroisoindolyl, 5,6,7,8-tetrahydroisoquinolinyl, pyridinyl, pyrimidinyl, furyl, thienyl, pyrrolyl, pyrazolyl, pyrrolidinyl, morpholinyl, piperazinyl, piperidinyl, and pyrrolidinyl. “Aryl” or “heteroaryl” means a stable 5- or 6-membered monocyclic or polycyclic ring containing 1 to 4, or preferably 1 to 3 heteroatoms selected from N, O, and S, with the remaining ring atoms being carbon. When the total number of S and O atoms in the heteroaryl group exceeds 1, these heteroatoms are not adjacent to each other. Preferably the total number of S and O atoms in the heteroaryl group is not greater than 2. It is particularly preferred that the total number of S and O atoms in the heteroaryl group is not greater than 1. The nitrogen atom in a heterocyclic ring may optionally be quaternized. When indicated, these heteroaryl groups can also be substituted with carbon or non-carbon atoms or groups. Such substitution may include the fusion with a 5 to 7-membered saturated cyclic group optionally containing 1 or 2 heteroatoms independently selected from N, O and S to form for example [1,3]dioxazo[4,5-c]pyridinyl. Examples of heteroaryl groups include, but are not limited to, pyridinyl, indolyl, pyrimidinyl, pyridizinyl, pyrazinyl, imidazolyl, oxazolyl, furyl, phenylthio, thiazolyl, triazolyl, tetrazolyl, isoxazolyl, quinolinyl, pyrrolyl, pyrazolyl, benz[b]thiophenyl, isoquinolinyl, quinazolinyl, quinoxalinyl, thienyl, isoindolyl, and 5,6,7,8-tetrahydroisoquinolinyl. “Pharmaceutically acceptable salt” or “salt of the compound” is a derivative of the disclosed compound, where the parent compound is modified by preparing a non-toxic acid or base addition salt thereof, and also refers to a pharmaceutically acceptable solvate, including a hydrate, of the compound and salt. Examples of pharmaceutically acceptable salts include, but are not limited to: inorganic or organic acid addition salts of basic residues such as amines; inorganic or organic base addition salts of acidic residues such as carboxylic acids; and a combination of one or more of the above salts. Pharmaceutically acceptable salts include non-toxic salts and quaternary ammonium salts of the parent compound formed, or example, with non-toxic inorganic or organic acids. For example, non-toxic acid salts include those derived from inorganic acids, such as: hydrochloric acid, hydrobromic acid, sulfuric acid, sulfamic acid, phosphoric acid, and nitric acid. Other acceptable inorganic salts include metal salts such as sodium salt, potassium salt, and cesium salts; alkaline earth metal salts such as calcium salts, and magnesium salts; and combinations including one or more of the above salts. The organic salts of the compounds include salts prepared with organic acids such as acetic acid, trifluoroacetic acid, propionic acid, succinic acid, glycolic acid, stearic acid, lactic acid, malic acid, tartaric acid, citric acid, ascorbic acid, embonic acid, maleic acid, hydroxymaleic acid, phenylacetic acid, glutamic acid, benzoic acid, salicylic acid, methanesulfonic acid, ethanesulfonic acid, benzenesulfonic acid, p-aminobenzenesulfonic acid, 2-acetoxybenzoic acid, fumaric acid, p-toluenesulfonic acid, methanesulfonic acid, ethanedisulfonic acid, oxalic acid, isethionic acid, and HOOC—(CH2)n-COOH; organic amine salts, such as triethylamine salt, pyridine salt, picoline salt, ethanolamine salt, triethanolamine salt, dicyclohexylamine salt, and N,N′-dibenzylethylenediamine salt; amino acid salts, such as: arginine salt, aspartate salt, and glutamate salt; and combinations of one or more of the above salts. “Glycosyl” includes monoglycosyl, diglycosyl, oligoglycosyl, and polyglycosyl, etc. Monoglycosyl includes, but is not limited to, erythrosyl, threitolyl, arabinosyl, ribosyl, xylosyl, lyxosyl, glucosyl, mannosyl, fructosyl, galactosyl, etc. Diglycosyl includes, but is not limited to, sucrosyl, maltosyl, cellobiosyl, isomaltosyl, gentiobiosyl, trehalosyl and lactosyl. “Prodrug” refers to a compound that is metabolized, for example by hydrolysis or oxidation, in the host to produce a compound of the present invention. Typical examples of the prodrug include compounds that have a biologically unstable protective group on the functional group of the active compound. The prodrug can be oxidized, reduced, aminated, deaminated, hydroxylated, dehydroxylated, hydrolyzed, dehydrated, alkylated, dealkylated, acylated, deacylated, phosphorylated, dephosphorylated to produce an active compound. “Derivative” refer to a more complex product derived from the substitution of hydrogen atom(s) or atomic group(s) of the compound with additional atom(s) or atomic group(s). Part DETAILED DESCRIPTION: The present invention will be further described by way of examples below; however, the present invention is not limited thereto. In examples below where no specific conditions are given in the experimental methods, the experimental conditions are selected according to conventional methods and conditions, or according to the product instructions. Route A: Synthesis of Compounds TG-001, TG-002, TG-003, TG-004, TG-005, TG-006, TG-007, TG-008, and TG-057 Experimental operations of Route a: Compound 4a (1 eq), Pd(PPh3)2Cl2 (2 mol %), and CuI (2 mol %) were added to a reaction flask. Under a N2 atmosphere, THF (0.2 M), Compound 5 (1.2 eq), and Et3N (9.6 eq) were sequentially added to the system, and then reacted for 20 h at room temperature. After filtering through celite (Shanghai Dahe Chemical Co., Ltd. analytical pure AR), the reaction solution was directly spin-dried, and then separated by chromatography (petroleum ether/ethyl acetate=2:1), to obtain Compound 6a (yield 89%). Compound 6a (1 eq), and Pd/C (10%) were added to MeOH (0.1 M), and reacted at room temperature for 20 h under 60 atm of H2. After filtering through celite, the reaction solution was concentrated under reduced pressure and purified by column chromatography on silica gel to obtain Compound 7a (yield 94%). 33% HBr/AcOH (4 eq) solution was added dropwise to Compound 8a (1 eq), and reacted at room temperature for 4 h. The reaction solution was directly spin-dried, and recrystallized in Et2O and n-hexane to obtain Compound 9a (76 g, yield 98%). Compounds 7a (1 eq) and 9a (1.2 eq) were added to a reaction flask. Under a N2 atmosphere, dichloromethane (0.3 M) was added to the system, and reacted for 30 min at room temperature. Ag2CO3 (1.2 eq) was added to the system, and reacted at room temperature for 20 h. After filtration, the reaction solution was directly spin-dried and separated by chromatography (Eluent: petroleum ether/ethyl acetate=4:1) to obtain Compound 10a (yield 40%). Compound 10a (1 eq) was added to a reaction flask, and then MeOH (4 M), H2O (4 M), and Et3N (2 eq) were respectively added, reacted at room temperature for 20 h, concentrated under reduced pressure, and purified by column chromatography on silica gel (Eluent: dichloromethane:methanol=9:1), to obtain Compound TG-001 (yield 70%). Compounds TG-002, TG-003, TG-004, TG-005, TG-006, TG-007, TG-008, and TG-057 have a synthesis route similar to that for Compound TG-001, and have structures show below: The identification data for structures of Compounds TG-001, TG-002, TG-003, TG-004, TG-005, TG-006, TG-007, TG-008, and TG-057 are shown below: Identification data for TG-001: 1H NMR (400 MHz, CD3OD) δ (ppm) 7.17-7.06 (m, 2H), 6.88 (d, J=8.0 Hz, 1H), 6.82 (td, J=7.4, 0.9 Hz, 1H), 4.23 (d, J=7.8 Hz, 1H), 3.91 (m, 1H), 3.85 (dd, J=11.9, 2.0 Hz, 1H), 3.80 (s, 3H), 3.66 (dd, J=11.9, 5.3 Hz, 1H), 3.55 (m, 1H), 3.37-3.21 (m, 3H), 3.19-3.12 (m, 1H), 2.61 (t, J=7.0 Hz, 2H), 1.64 (m, 4H). LRMS (ESI): [M+Na]+ 365.1; HRMS (ESI): [M+H]+ calculated C17H27O7+ 343.1751, found 343.1748. Data for TG-002 1H NMR (400 MHz, CD3OD) δ (ppm) 6.35 (d, J=2.2 Hz, 2H), 6.28 (t, J=2.2 Hz, 1H), 4.24 (d, J=7.8 Hz, 1H), 3.96-3.91 (m, 1H), 3.85 (dd, J=11.8, 1.7 Hz, 1H), 3.74 (s, 6H), 3.66 (dd, J=11.9, 5.2 Hz, 1H), 3.58-3.53 (m, 1H), 3.38-3.21 (m, 3H), 3.19-3.11 (m, 1H), 2.57 (t, J=7.3 Hz, 2H), 1.75-1.58 (m, 4H). LRMS (ESI): [M+Na]+ 395.1; HRMS (ESI): [M+NH4]+ calculated C18H32O8N+ 390.2122, found 390.2122. Data for TG-003 1H NMR (400 MHz, CD3OD) δ (ppm) 6.84 (d, J=8.2 Hz, 1H), 6.79 (d, J=1.9 Hz, 1H), 6.72 (dd, J=8.1, 1.9 Hz, 1H), 4.24 (d, J=7.8 Hz, 1H), 3.98-3.88 (m, J H), 3.86 (dd, J=11.9, 1.9 Hz, 1H), 3.81 (s, 3H), 3.79 (s, 1H), 3.66 (dd, J=11.9, 5.3 Hz, 1H), 3.61-3.51 (m, 1H), 3.38-3.21 (m, 3H), 3.20-3.12 (m, 1H), 2.58 (t, J=7.2 Hz, 2H), 1.75-1.56 (m, 4H). LRMS (ESI): [M+Na]+ 395.1; HRMS (ESI): [M+NH4]+ calculated C18H32O8N+ 390.2122, found 390.2118. Data for TG-005: 1H NMR (400 MHz, CD3OD) δ (ppm) 7.07 (d, J=8.8 Hz, 2H), 6.80 (d, J=8.8 Hz, 2H), 4.23 (d, J=7.8 Hz, 1H), 3.93-3.82 (m, 2H), 3.75 (s, 3H), 3.66 (dd, J=11.9, 5.3 Hz, 1H), 3.52 (dt, J=9.5, 6.7 Hz, 1H), 3.38-3.22 (m, 3H), 3.20-3.12 (m, 1H), 2.54 (t, J=7.6 Hz, 2H), 1.68-1.61 (m, 4H), 1.47-1.31 (m, 2H). LRMS (ESI): [M+Na]+ 375.1; HRMS (ESI): [M+H]+ calculated C18H29O7+ 357.1908, found 357.1906. Data for TG-006: 1H NMR (400 MHz, CD3OD) δ (ppm) 7.06 (d, J=8.6 Hz, 2H), 6.84-6.80 (d, J=8.6 Hz, 2H), 4.23 (d, J=7.8 Hz, 1H), 3.93-3.82 (m, 2H), 3.75 (s, 3H), 3.66 (dd, J=11.9, 5.2 Hz, 1H), 3.52 (dt, J=9.5, 6.7 Hz, 1H), 3.38-3.21 (m, 3H), 3.20-3.11 (m, 1H), 2.53 (t, J=7.6 Hz, 2H), 1.68-1.50 (m, 4H), 1.47-1.25 (m, 4H). LRMS (ESI): [M+Na]+ 393.1; HRMS (ESI): [M+NH4]+ calculated C19H34O7N+ 388.2330, found 388.2327. Data for end product TG-004: 1H NMR (400 MHz, CD3OD) δ (ppm) 7.15 (t, J=7.8 Hz, 1H), 6.79-6.67 (m, 3H), 4.24 (d, J=7.8 Hz, 1H), 3.92 (dt, J=9.4, 6.4 Hz, 1H), 3.85 (dd, J=11.9, 1.8 Hz, 1H), 3.76 (s, 3H), 3.66 (dd, J=11.9, 5.2 Hz, 1H), 3.60-3.51 (m, 1H), 3.39-3.21 (m, 3H), 3.19-3.12 (m, 1H), 2.60 (t, J=7.3 Hz, 2H), 1.78-1.56 (m, 4H). LRMS (ESI): [M+Na]+ 365.1; HRMS (ESI): [M+NH4]+ calculated C7H30O7N+ 360.2017, found 360.2016. Data for TG-007: 1H NMR (400 MHz, CD3OD) δ (ppm) 6.49 (s, 2H), 4.24 (d, J=7.8 Hz, 1H), 3.97-3.83 (m, 2H), 3.81 (s, 6H), 3.72 (s, 3H), 3.69-3.52 (m, 2H), 3.37-3.21 (m, 3H), 3.20-3.13 (m, 1H), 2.59 (t, J=7.3 Hz, 2H), 1.79-1.55 (m, 4H). LRMS (ESI): [M+Na]+ 425.1; HRMS (ESI): [M+NH4]+ calculated C19H34O9N+ 420.2228, found 420.2226. Data for TG-008: 1H NMR (400 MHz, CD3OD) δ (ppm) 6.71-6.67 (m, 2H), 6.65-6.61 (m, 1H), 5.87 (s, 2H), 4.23 (d, J=7.8 Hz, 1H), 3.95-3.88 (m, 1H), 3.85 (m, 1H), 3.66 (dd, J=11.8, 5.2 Hz, 1H), 3.60-3.48 (m, 1H), 3.38-3.20 (m, 3H), 3.19-3.12 (m, 1H), 2.55 (t, J=7.1 Hz, 2H), 1.73-1.53 (m, 4H). LRMS (ESI): [M+Na]+ 379.0; HRMS (ESI): [M+Na]+ calculated C17H24O8Na+ 379.1374, found 379.1362. Data for TG-057 1H NMR (400 MHz, CDCl3) δ (ppm) 6.83 (d, 1H, J=7.6 Hz), 6.70-6.64 (m, 2H), 6.26 (br, 1H), 4.83 (br, 8H), 4.00 (s, 1H), 3.88 (s, 3H), 3.74 (t, 2H, J=6.4 Hz), 3.55 (s, 2H), 2.58 (t, 2H, J=7.2 Hz), 1.69-1.62 (m, 4H). LRMS (ESI): [M+Na]+ 381.2. The structure of each reaction intermediate during the experiment is shown below: The identification data for Intermediates 10a-10h is: 10a: 1H NMR (400 MHz, CDCl3) δ 6.32 (d, J=2.2 Hz, 2H), 6.29 (t, J=2.2 Hz, 1H), 5.20 (t, J=9.5 Hz, 1H), 5.08 (t, J=9.7 Hz, 1H), 4.98 (dd, J=9.6, 8.0 Hz, 1H), 4.48 (d, J=8.0 Hz, 1H), 4.26 (dd, J=12.3, 4.7 Hz, 1H), 4.13 (dd, J=12.3, 2.3 Hz, 1H), 3.89 (d, J=9.5 Hz, 1H), 3.78 (s, 6H), 3.68 (dd, J=9.9, 2.2 Hz, 1H), 3.49 (d, J=9.4 Hz, 1H), 2.55 (t, J=6.6 Hz, 2H), 2.08 (s, 3H), 2.05-1.97 (m, 9H), 1.63 (dd, J=11.5, 4.3 Hz, 4H). LRMS (ESI): [M+Na]+ 533.5. 10b: 1H NMR (400 MHz, CDCl3) 6.34-6.28 (m, 3H), 5.20 (t, J=9.5 Hz, 1H), 5.08 (t, J=9.7 Hz, 1H), 4.98 (dd, J=9.6, 8.0 Hz, 1H), 4.48 (d, J=8.0 Hz, 1H), 4.26 (dd, J=12.3, 4.7 Hz, 1H), 4.13 (dd, J=12.3, 2.3 Hz, 1H), 3.89 (d, J=9.5 Hz, 1H), 3.78 (s, 6H), 3.68 (dd, J=9.9, 2.2 Hz, 1H), 3.49 (d, J=9.4 Hz, 1H), 2.55 (t, J=6.6 Hz, 2H), 2.10-2.07 (s, 3H), 2.03 (s, 3H), 2.00 (m, 6H), 1.63 (dd, J=11.5, 4.3 Hz, 4H). LRMS (ESI): [M+Na]+ 563.5. 10c: 1H NMR (300 MHz, CDCl3) δ 6.82-6.59 (m, 3H), 5.27-4.83 (m, 3H), 4.46 (d, J=7.9 Hz, 1H), 4.32-3.99 (m, 2H), 3.83 (m, 7H), 3.74-3.35 (m, 2H), 2.53 (m, 2H), 1.99 (m, 12H), 1.59 (m, 4H). LRMS (ESI): [M+Na]+ 563.5. 10d: 1H NMR (300 MHz, CDCl3) δ 7.19 (t, J=8.1 Hz, 1H), 6.81-6.65 (m, 3H), 5.28-4.88 (m, 3H), 4.48 (d, J=8.0
{'bibliographic_information': "{'country': 'US', 'doc-number': '17054124', 'kind': 'B2', 'date': '20190507', 'invention_title': 'Glycoside compound and preparation method therefor, composition, application, and intermediate'}", 'source_file': './grant/2022/ipg220510.xml', 'source_data': 'USPTO-Grant'}