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. Author manuscript; available in PMC: 2021 May 1.
Published in final edited form as: Neurobiol Aging. 2019 Dec 16;89:41–54. doi: 10.1016/j.neurobiolaging.2019.12.009

Fig. 5.

Fig. 5.

The ROCK inhibitor (H1152) inactivated caspase-3 and activated BCL-2 in M1C cells. (A) The amount of cleaved caspase-3 was reduced by the ROCK inhibitor. 0: 0 μM ROCK inhibitor,1: 1 μM ROCK inhibitor, 10: 10 μM ROCK Inhibitor. N = 4, **p < 0.01, Bar: ± SD. (B) Bcl-2 activation was also observed after ROCK inhibitor treatment, N = 3, **p < 0.01, Bar: ± SD. Caspase-cleaved tau was reduced by ROCK inhibitor treatment, as shown by Western blotting (N = 4), **p < 0.01, Bar: ± SD (C), and immnocytochemical study. N = 4, **p < 0.01, Bar: ± SD, Scale 75 μM (D). Data from cleaved caspase3/GAPDHP, TauC3/GAPDH, and BCL2/GAPDH followed a normal distribution and were analyzed with one-way ANOVA followed by Bonferroni post hoc test. The immunocytochemical data from TauC3 followed a normal distribution and were analyzed with Student’s t-test. Abbreviations: CC3, cleaved caspase-3; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; ROCK, Rho-associated coiled-coil protein kinase.