ClC-3 chloride channel in hippocampal neuronal apoptosis
Lijuan Xu
Shuling Zhang
Hongling Fan
Zhichao Zhong
Xi Li
Xiaoxiao Jin
Quanzhong Chang
摘要：Over-production of nitric oxide is pathogenic for neuronal apoptosis around the ischemic area fol-lowing ischemic brain injury. In this study, an apoptotic model in rat hippocampal neurons was tablished by 0.5 mmol/L 3-morpholinosyndnomine (SIN-1), a nitric oxide donor. The models were then cultured with 0.1 mmol/L of 4,4’-di sothiocyanostilbene-2,2’-disulfonic acid (DIDS;the chloride channel blocker) for 18 hours. Neuronal survival was detected using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and apoptosis was assayed by Hoechst 33342-labeled neuronal DNA fluorescence staining. Western blot analysis and immunoche-nescence staining were applied to determine the changes of activated caspase-3 and CIC-3 channel proteins. Real-time PCR was used to detect the mRNA expression of CIC-3. The results showed that SIN-1 reduced the neuronal survival rate, induced neuronal apoptosis, and promoted ClC-3 chloride channel protein and mRNA expression in the apoptotic neurons. DIDS reversed the effect of SIN-1. Our findings indicate that the increased activities of the ClC-3 chloride channel may be involved in hippocampal neuronal apoptosis induced by nitric oxide.
机标关键词：neuronal apoptosischloride channelnitric oxidemRNA expressionischemic brain injuryhippocampal neuronssurvival rate
资助基金：the National Natural Science Foundation of China, (No.81160157)a grant from Guizhou Science and Technology Department in China, (No. SY20093075)Technological Talents Funds of Guizhou Province in China, (No.201209)
论文发表日期：2013-01-01
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：8( 3047-3054 )
英文信息