neuroprotective effects of exogenous activin a on oxygen-glucose deprivation in pc12 cells神经保护作用的外源性苯丙酸诺龙在pc12细胞oxygen-glucose剥夺.pdfVIP

Molecules 2012, 17, 315-327; doi:10.3390/molecule OPEN ACCESS molecules ISSN 1420-3049 /journal/molecules Article Neuroprotective Effects of Exogenous Activin A on Oxygen-Glucose Deprivation in PC12 Cells Jin-Ting He 1, Jing Mang 1, Chun-Li Mei 1,2, Le Yang 3, Jiao-Qi Wang 1, Ying Xing 1, Hong Yang 1 and Zhong-Xin Xu 1,* 1 Department of Neurology, China-Japan Friendship Hospital, Jilin University, Changchun 130012, China; E-Mails: Hejinting333@ (J.-T.H.); Mangjing505@ (J.M.); wangjiaoqi111@ (J.-Q.W.); xingying333@ (Y.X.); yanghong555@ (H.Y.) 2 College of Nursing, Beihua University, Jilin 132013, China; E-Mail: meixiaoqing2007@126.com 3 People’s Hospital of Jilin Province, Changchun 130021, China; E-Mail:Yangle800511@ * Author to whom correspondence should be addressed; E-Mail: xuzhongxin999@; Tel.: +86-431-8464-5107; Fax: +86-431-8464-5107. Received: 6 December 2011; in revised form: 19 December 2011 / Accepted: 22 December 2011 / Published: 30 December 2011 Abstract: Ischemic cerebrovascular disease is one of the most common causes of death in the World. Exogenous activin A (ActA) protects neurons against toxicity and plays a central role in regulating the brain’s response to injury. In the present study, we investigated the mechanisms involved in the neuroprotective effects of ActA in a model of hypoxic-ischemic brain disease. We found that ActA could effectively increase the survival rate of PC12 cells and relieve oxygen-glucose deprivation