摘要
目的:探讨PI3K/Akt信号通路在米诺环素(minocycline,MC)抑制硝普钠(sodium nitoprusside,SNP)诱导的PC12细胞凋亡中的作用。方法:将体外培养的PC12细胞分为4组:空白对照组、SNP组、MC+SNP组和PI3K抑制剂LY294002+MC+SNP组。用四甲基偶氮唑盐(MTT)法检测细胞活力,流式细胞术检测细胞凋亡;Western blotting检测不同时点(0.5、1、2、3 h)各处理组PI3K/Akt通路蛋白p-Akt和Akt的表达。结果:SNP处理PC12细胞24 h能抑制细胞生长,加入10μmol/L MC预处理30 min可明显提高细胞活力,降低细胞凋亡率(P<0.05),抑制SNP诱导的PC12细胞凋亡。MC组的p-Akt表达高于其它组,而加入LY294002后可阻断MC的上述效应。结论:MC可通过调控PI3K/Akt通路抑制SNP诱导的PC12细胞凋亡。
AIM： To explore the role of PI3 K/Akt signaling in the anti-apoptotie effect of minecyline （MC） on the apoptosis of PC12 cells induced by sodium nitroprusside （SNP）. METHODS： PC12 cells were divided into 4 groups： blank control Sreup, SNP （500 p^mol/L） group, MC （10 trmol/L） ＋ SNP group and LY294002 ＋ MC ＋ SNP group. The cell viability was observed by MTF assay. The expression of Akt and p-Akt was determined by Western blotting. RE- SULTS： The viability of the PC12 cells decreased after exposed to 500 p^mol/L SNP for 24 h. Meanwhile, MC at concen- tration of 10 ~mol/L significantly blocked the effect of SNP, such as decreasing the cell viability. Pretreatment with LY294002 for 60 min prior to exposure of the PC12 cells to MC and SNP down-regnlated the expression of p-Akt induced by SNP. CONCLUSION： Minecycline regulates PI3K/Akt signaling pathway to restrain the apoptosis of PC12 cells induced by SNP.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2013年第4期660-663,共4页
Chinese Journal of Pathophysiology
基金
广东省自然科学基金资助项目(No.S2011010004626)
