机构：[1]Anatomy Department, Changzhi Medical College, Changzhi, Shanxi,[2]Key Laboratory of Tissue Regeneration of Henan Province, Xinxiang Medical University, Xinxiang, Henan,[3]Clinical Laboratory of Heji Hospital Affiliated to Changzhi Medical College, Changzhi, Shanxi,[4]Department of Nuclear Medicine, Xuanwu Hospital, Capital Medical University, Beijing,首都医科大学宣武医院[5]Department of Physiology, Shanxi Medical University, Taiyuan, Shanxi,[6]Department of Radiology, China-Japan Friendship Hospital, Beijing,[7]Department of Radiology, First Clinical Medical College, Shanxi Medical University, Taiyuan, Shanxi, People’s Republic of China[8]School of Medicine, University of California – San Diego, San Diego, CACA, USA
N-methyl-D-aspartate (NDMA) receptor-mediated excitotoxicity has been implicated in a variety of pathological situations such as Alzheimer's disease (AD) and Parkinson's disease. However, no effective treatments for the same have been developed so far. Humanin (HN) is a 24-amino acid peptide originally cloned from the brain of patients with AD and it prevents stress-induced cell death in many cells/tissues. In our previous study, HN was found to effectively rescue rat cortical neurons. It is still not clear whether HN protects the neurons through the attenuation of mitochondrial dysfunction. In this study, excitatory toxicity was induced by NMDA, which binds the NMDA receptor in primarily cultured rat cortical neurons. We found that NMDA (100 mu mol/L) dramatically induced the decrease of cell viability and caused mitochondrial dysfunction. Pretreatment of the neurons with HN (1 mu mol/L) led to significant increases of mitochondrial succinate dehydrogenase (SDH) activity and membrane potential. In addition, HN pretreatment significantly reduced the excessive production of both reactive oxygen species (ROS) and nitric oxide (NO). Thus, HN could attenuate the excitotoxicity caused by the overactivation of the NMDA receptor through the alleviation of mitochondrial dysfunction.
基金：
The National Key Research and Development Program of China (no 2016YFC0100105),
the National Science Foundation of China (nos 81628008, 81571641, and 81471652),
internal grant from the China-Japan Friendship Hospital, Beijing, People’s Republic of China (no 2014-3-MS-18).
第一作者机构：[1]Anatomy Department, Changzhi Medical College, Changzhi, Shanxi,
通讯作者：
通讯机构：[*1]Department of Radiology, China-Japan Friendship Hospital, No. 2 Yinghua Dongjie, Chaoyang District, Beijing, 100029, People’s Republic of China[*2]Key Laboratory of Tissue Regeneration of Henan Province, Xinxiang Medical University, East Jinsui Road, Xinxiang, Henan 453003, People’s Republic of China
推荐引用方式(GB/T 7714)：
Ai-Ling Cui ,Ying-Hua Zhang ,Jian-Zhong Li ,et al.Humanin rescues cultured rat cortical neurons from NMDA-induced toxicity through the alleviation of mitochondrial dysfunction[J].DRUG DESIGN DEVELOPMENT AND THERAPY.2017,11:1243-1253.doi:10.2147/DDDT.S133042.
APA：
Ai-Ling Cui,,Ying-Hua Zhang,,Jian-Zhong Li,,Tianbin Song,,Xue-Min Liu,...&Kefeng Li.(2017).Humanin rescues cultured rat cortical neurons from NMDA-induced toxicity through the alleviation of mitochondrial dysfunction.DRUG DESIGN DEVELOPMENT AND THERAPY,11,
MLA：
Ai-Ling Cui,,et al."Humanin rescues cultured rat cortical neurons from NMDA-induced toxicity through the alleviation of mitochondrial dysfunction".DRUG DESIGN DEVELOPMENT AND THERAPY 11.(2017):1243-1253
