TRPC1缺失对小鼠脑神经细胞生存的影响  

Effect of TRPC1 depletion on survival of cerebral nerve cells

作　　者：幸仁忠 刘建军[2] 许华[1] 杨细飞[2] 

机构地区：[1]暨南大学药学院,广东广州510632 [2]深圳市疾病预防控制中心,深圳市现代毒理学重点实验室,广东深圳518055

出　　处：《中国病理生理杂志》2016年第4期686-690,共5页Chinese Journal of Pathophysiology

基　　金：广东省自然科学基金资助项目(No.2014A030313715);深圳市科技研发基金基础研究项目(No.JCYJ20130329103949650)

摘　　要：目的:研究瞬时受体电位通道1(TRPC1)缺失对小鼠海马神经元生存的影响。方法:选用6月龄TRPC1基因敲除小鼠及其对照小鼠,通过神经元特异性标志物Neu N免疫染色、尼氏染色及TUNEL染色检测TRPC1敲除小鼠海马CA1、CA3及齿状回(DG)神经细胞的变化情况。通过Western blot检测TRPC1基因敲除小鼠促凋亡因子C/EBP同源蛋白(C/EBP homologous protein,CHOP)及凋亡相关蛋白cleaved caspase-3的表达水平。结果:Neu N免疫荧光和尼氏染色发现,TRPC1基因敲除小鼠海马CA1、CA3及DG区神经细胞显著减少;TUNEL染色检测发现TRPC1基因敲除小鼠以上区域神经细胞凋亡显著增加;Western blot结果显示,与对照小鼠相比,TRPC1基因敲除小鼠海马组织CHOP及cleaved caspase-3的水平均显著升高。结论:TRPC1基因缺失可导致小鼠海马神经元数量显著减少,其机制可能与TRPC1缺失促进神经细胞凋亡有关。AIM： To study the effect of transient receptor potential channel 1（ TRPC1） on the survival of hippocampal neurons in mice. METHODS： TRPC1 knockout mice and the control mice（ 6 months old） were used in this study. Immunofluorescence staining of neuron-specific marker Neu N,Nissl staining and TUNEL staining were performed to measure the changes of the neurons in hippocampal CA1,CA3 and dentate gyrus（ DG）. Western blot analysis was used to detect the levels of pro-apoptotic protein C / EBP homologous protein（ CHOP） and cleaved caspase-3. RESULTS： Immunofluorescence staining and Nissl staining showed that the number of neuronal cells was significantly decreased in hippocampal CA1,CA3 and DG of TRPC1 knockout mice compared with the control mice. TUNEL staining showed that the apoptosis neuronal cell number of the above areas in TRPC1 knockout mice was significantly increased compared with the control mice. The results of Western blot revealed that the levels of CHOP and cleaved caspase-3 were significantly increased in the hippocampus of TRPC1 knockout mice relative to the control mice. CONCLUSION： The depletion of TRPC1 induces neuronal loss through a mechanism of TRPC1-mediated apoptosis.

关 键 词：瞬时受体电位通道1 神经元 C/EBP同源蛋白 CASPASE-3 

分 类 号：R363[医药卫生—病理学]