Cytochalasin B in cell movement
The other inhibitors work on other processes, as you already noticed. There is almost no difference between the conditions when they are added and the corresponding condition when they are missing, suggesting those other processes play no role in the observed phenomenon. Eliminating those other processes makes it more believable that actin polymerization is important, rather than being one of multiple factors.

Moreover, often cell will adapt to an inhibitor by increasing or decreasing other kinds of activity. For example, it could be that actin polymerization inhibition prevents amoeba from eating. In this case, because any imaginable motive mechanism requires energy, starving amoeba may become unable to move, even though it was not using actin for movement. In order to refute such scenarios, where actin polymerization is not directly inducing movement, and where cytochalazine does not inhibit movement directly mechanism, supplementary experiments were performed.

DNP induces something similar to starvation, yet, in these experiments, did not abolish movements when given alone. Nor did DNP rescue movement, because the combination (DNP + cytochalazine) is virtually identical to cytochalazine alone. In both circumstances, DNP did nothing, thus showing that ATP depletion is not influencing movement. This is proof that actin polymerization is directly causing amoeba movement, and not an indirect ATP-mediated effect. Similarly, cytochalazin's effect is independent of protein synthesis, once more supporting the hypothesis that actin polymerization is important on its own.