Mfn1‐mediated mitochondrial protection system is activated by resveratrol in the presence of hypoxia‐reoxygenation (HR) injury. A‐B, Western blotting was used to observe the alterations of Mfn1 expression in response to HR injury and/or resveratrol treatment. Besides, siRNA against Mfn1 was transfected into N2a cell and the knockdown efficiency of N2a cell was determined via Western blotting. C, Cell viability was measured via MTT assay. D, Lactate dehydrogenase (LDH) release assay was used to verify the cell death in response to Mfn1 knockdown. E, Adenosine triphosphate (ATP) production was detected via ELISA. Resveratrol was added into the medium of N2a cell at low and high dose. N2a cell was treated with HR injury. F, Caspase‐9 activity was measured to reflect the mitochondrial damage in response to Mfn1 deletion. *P < .05 vs control group; #
P < .05 vs HR group; @
P < .05 vs HR + Res group