氯胺酮诱导大鼠海马神经元凋亡及机制

目的 研究氯胺酮对SD大鼠海马神经元的凋亡诱导作用,并探究其作用机制.方法 培养SD大鼠海马神经元细胞,将对数生长期的大鼠海马神经元分为对照组(不加氯胺酮)和实验组(加氯胺酮且其终浓度分别为10、20 μmol/L).24h后,缩胆囊素8肽(CCK-8)法检测细胞存活率,流式细胞术检测细胞凋亡,蛋白质印迹法检测蛋白phospho-细胞外信号调节蛋白激酶(P-ERK)、Bax、Bcl-2的表达.结果 10、20 μmol/L实验组神经元的存活率分别为(73.7±1.5)％和(58.2±2.4)％,明显低于对照组的(97.2±1.8)％(P＜0.05)；凋亡率分别为(24.5±7.4)％和(34.7±4.9)％,明显高于对照组的(4.7±2.3)％(P＜0.05)；P-ERK、Bax表达量增加,Bcl-2表达量减少.结论 氯胺酮能够诱导大鼠海马神经元凋亡,可能是通过激活P-ERK、改变Bax/Bcl-2比值实现的.

The effect and the mechanism of apoptosis of hippocampal neural cells induced by the ketamine in Sprague Dawley rat

Objective To study the effect and the mechanism of apoptosis of hippocampal neural cells induced by the ketamine in Sprague Dawley(SD) rat.Methods Cortical neurons were isolated from newborn SD rats and were divided into control group and experimental group.Control group was given regular treatment and experimental group was treated with ketamine ( 10,20 μmol/L).After 24 h,the index including cell survival rate,apoptosis rate and the expressive rate of phospho-extracellular signal-regulated kinase ( P-ERK),Bax and Bcl-2 were tested by using CCK-8,FCM and Western blot,respectively.Results Cell survival rates were (73.7 ± 1.5 ) ％ and (58.2 ± 2.4) ％ with 10 μmol/L or 20 μmol/L ketamine treatment,which was.significantly decreased ( P ＜ 0.05 )compared with control group(97.2 ± 1.8) ％.Cell apoptosis rates was (24.5 ± 7.4) ％ and ( 34.7 ± 4.9) ％ with 10 μmol/L or 20 μmol/L ketamine treatment,which also was significantly increased( P ＜0.05)compared with control group (4.7 ± 2.3) ％.The expressions of P-ERK and Bax were increased,while the expressions of Bcl-2 was decreased.Conclusion The ketamine can induce apoptosis in SD rat hippocampal neural cells,which might be involved in activating P-ERK and changing the rate of BAX/BCL-2.