• Dujuan Sha, Luna Wang, Jun Zhang, Lai Qian, Qiming Li, Jin Li, Jian Qian, Shuangshuang Gu, Ling Han, Peng Xu, and Yun Xu.
• Department of Emergency, Nanjing Drum Tower Hospital Affiliated to Nanjing University Medical School, Nanjing 210008, Jiangsu Province, China; Department of Emergency, Drum Tower Clinical Medical School, Nanjing Medical University, Nanjing 210008, Jiangsu Province, China; The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, China.
• Brain Res. 2014 Sep 25;1582:107-13.

AbstractThe mechanisms of ischemic stroke, a main cause of disability and death, are complicated. Ischemic stroke results from the interaction of various factors including oxidative stress, a key pathological mechanism that plays an important role during the acute stage of ischemic brain injury. This study demonstrated that cocaine- and amphetamine-regulated transcript (CART) peptide, specifically CART55-102, increased the survival rate, but decreased the mortality of neurons exposed to oxygen-glucose deprivation (OGD), in a dose-dependent manner. The above-mentioned effects of CART55-102 were most significant at 0.4nM. These results indicated that CART55-102 suppressed neurotoxicity and enhanced neuronal survival after oxygen-glucose deprivation. CART55-102 (0.4nM) significantly diminished reactive oxygen species levels and markedly increased the activity of mitochondrial respiratory chain complex II in oxygen-glucose deprived neurons. In summary, CART55-102 suppressed oxidative stress in oxygen-glucose deprived neurons, possibly through elevating the activity of mitochondrial respiratory chain complex II. This result provides evidence for the development of CART55-102 as an antioxidant drug.Copyright © 2014 Elsevier B.V. All rights reserved.

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