Figure 7.

Effect of NAC-replenishing on emodin-induced ER stress, mitochondrial dysfunction and apoptosis in T cells. Replenishing of 20 μmol/L exogenous NAC significangly reduced the ROS (A) and MDA (C) production induced by 100 μmol/L emodin, and elevated antioxidant SOD level (B). NAC replenishing also rescued ER stress (G and H), Ca²⁺ release (D), disruption of ΔΨm (E), mitochondrial dysfunction and cytochrome c release (I and J) induced by emodin, which finally inactivated caspases (K and L), and reduced apoptosis of T cells (F). The results are given as mean±SD from three experiments. ^bP<0.05, ^cP<0.01 vs control groups.