【摘要】 目的探讨TRPC离子通道通过p53通路参与一氧化氮供体硝普钠(SNP)诱导的原代培养海马神经元凋亡。方法原代培养的海马神经元,经RT-PCR检测TRPC1-6的表达;给予SNP处理后,通过Real-time RT-PCR检测p53下游靶基因Bax、Apaf-1、PUMA和Survivin的表达;给予TRPC通道阻断剂和激活剂,检测其是否影响SNP诱导的p53下游靶基因表达。结果 TRPC在原代培养海马神经元上广泛表达。SNP处理神经元4、8、24h后,p53下游靶基因Bax、Apaf-1和Survivin表达无明显变化(P>0.05)。而PUMA则在3个时间点分别增加至1.94、1.86和1.90倍,与对照组比较差异有统计学意义(P<0.01)。TRPC通道阻断剂2-APB,可降低SNP诱导的PUMA上调(1.91vs1.12)(P<0.01)。结论 TRPC通道可以通过调节PUMA的表达参与SNP诱导的原代培养海马神经元凋亡。更多还原

【Abstract】 Objective To determine whether canonical transient receptor potential channel(TRPC) is involved in SNPinduced apoptosis of the primary cultured rat hippocampal neurons via PUMA.Methods The cultured rat hippocampal neurons were treated with SNP.The expression of TRPC1-6 in hippocampal neurons were detected using RT-PCR.The expression level of Bax,Apaf-1,survivin and PUMA mRAN in hippocampal neurons were detected using Real-time RT-PCR.Results TRPCs were widely expressed in hippocampal neurons.The hippocampal neurons were treated with SNP for 4 h,8 h and 24 h,and SNP had no effect on the expression of Bax,Apaf-1 and survivin mRNA(P>0.05);However,the expression level of PUMA was significantly increased to 1.94(4 h),1.86(8 h) and 1.9-fold(24 h)(P<0.01).TRPC blocker(2-APB) was found to lower the elevated expression of PUMA(P<0.01).Conclusion TRPC channels are involved in SNP-induced apoptosis of cultured rat hippocampal neurons via PUMA.更多还原