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Carbocistein improves airway remodeling in asthmatic mice.

BACKGROUND
The alleviating effects of carbocisteine (S-carboxymethylcysteine, SCMC) have been implicated in chronic obstructive pulmonary disease; however, very little is known about its mechanisms in asthma. In this study, we aimed to investigate the effects of SCMC on airway remodeling in asthmatic mice induced by ovalbumin (OVA).


METHODS
The asthma mouse model was generated by OVA sensitization and stimulation and subsequently intervened by SCMC or dexamethasone. Bronchoalveolar lavage fluid (BALF) and lung tissues were collected from each group of mice. The TGF-β1 levels in BALF were measured by ELISA. Masson's staining was used to detect collagen fiber deposition in mouse airway tissues, while immunohistochemistry and RT-qPCR were conducted to examine the protein and mRNA expression of TGF-β1 in mouse lung airway tissues, respectively. The correlation between TGF-β1 mRNA expression and the area of collagen fiber deposition in airway tissues was analyzed by Pearson's correlation coefficient.


RESULTS
The area of collagen fiber deposition in the airway tissues of asthmatic mice was significantly increased, while SCMC alleviated the collagen fiber deposition in the airway tissues. TGF-β1 expression was significantly elevated in BALF and airway tissues of asthmatic mice, while SCMC inhibited TGF-β1 expression. TGF-β1 expression was significantly and positively correlated with collagen fiber deposition in mouse airway tissues.


CONCLUSIONS
SCMC intervention improves collagen fiber deposition in airway tissues and inhibits TGF-β1 expression in asthmatic mice.