Figure 6.

Melatonin protects against oxidative stress by preserving the stability of parkin. (A) Expression of anti-apoptotic protein BCL2, and pro-apoptotic proteins BAX, C-caspase-3, and C-PARP-1, in hMSCs treated with melatonin (1 μM, 24 h) and HSPA1L siRNA (si-HSPA1L) (B) Expression levels were normalized relative to those of β-actin. Values represent the mean ± SEM. * p < 0.05, and ** p < 0.01 vs. untreated hMSCs, # p < 0.05, and ## p < 0.01 vs. H₂O₂-treated hMSCs, $ p < 0.05 vs. melatonin-treated hMSCs pretreated with si-HSPA1L. (C) hMSCs were pre-treated with melatonin (1 μM, 24 h) and si-HSPA1L, and subjected to oxidative stress. Untreated hMSCs were subjected to oxidative stress only. (D) All groups were assayed using PI-Annexin V, and Annexin V-positive hMSCs were quantified using FACS. Values represent the mean ± SEM. ** p < 0.01 vs. untreated hMSCs, ## p < 0.01 vs. melatonin-treated hMSCs, $$ p < 0.01 vs. melatonin-treated hMSCs pretreated with si-HSPA1L.