Figure 2.

Mitochondrial apoptosis is inhibited by resveratrol in N2a cell. A, Caspase‐9 activity was determined using ELISA. Resveratrol was added into the medium of N2a cell at low and high dose. N2a cell was treated with hypoxia‐reoxygenation (HR) injury. B‐F, Western blotting was performed to observe the changes in mitochondrial apoptosis‐related proteins. Pro‐apoptotic proteins such as Bax and caspase‐9 were upregulated in response to HR injury and were reduced to near‐normal levels with resveratrol treatment. In contrast, anti‐apoptotic proteins such as Bcl‐2 and survivin were inhibited by HR injury and were reversed to near‐normal levels with resveratrol treatment. G‐H, Immunofluorescence assay for cyt‐c translocation from cytoplasm into nucleus. The expression of nuclear cyt‐c was determined. I, Mitochondrial permeability transition pore (mPTP) opening rate was determined using ELISA, and the mPTP opening was negatively modulated by resveratrol in the setting of cerebral IR injury. *P < .05 vs control group; ^# P < .05 vs HR group