期刊
BRAIN AND BEHAVIOR
卷 9, 期 2, 页码 -出版社
WILEY
DOI: 10.1002/brb3.1200
关键词
cerebral ischemia; leptin; mitochondria; neuroprotection; STAT3
资金
- University Scientific Research Program of Guangxi Zhuang Autonomous Region Education Department [YB2014069]
- Medical Health Appropriate Technology Research and Development Project of Guangxi Zhuang Autonomous Region Health and Family Planning Commission [S201656]
Background According to recent studies, leptin may exert a neuroprotective function by affecting the phosphorylation of signal transducer and activator of transcription 3 (STAT3). During stress, STAT3 regulates mitochondrial oxidative stress and reduces apoptosis. Objective In the present study, we hypothesized that leptin increases STAT3 phosphorylation in the mitochondria and protects against mitochondrial oxidative stress in rats subjected to permanent middle cerebral artery occlusion (MCAO). Results Leptin reduced reactive oxygen species (ROS) production, and we confirmed that the mechanism underlying this change involved the enzymatic activities of mitochondrial respiratory chain complexes I and II. In addition, leptin increased the level of STAT3 Ser727 phosphorylation in the mitochondria. Conclusions Based on these results, leptin may regulate mitochondrial respiratory chain enzymatic activities via mitochondria-targeted STAT3 to reduce ROS production and protect brain tissues from mitochondrial oxidative stress during cerebral ischemia.
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