盐酸戊乙奎醚对大鼠缺氧缺糖／复氧复糖海马脑片凋亡相关因子表达的影响

目的研究盐酸戊乙奎醚（penehyclidine hydrochloride，PHC）对大鼠缺氧缺糖／复氧复糖海马脑片的保护作用及机制。方法采用大鼠海马脑片缺氧缺糖／复氧复糖模型；分为正常组、缺氧缺糖／复氧复糖（H／R）组、PHC 2μmol／L（PHC2组）、PHC 10μmol／L（PHC10组）、PHC 50μmol／L（PHC 50组）、Sco 50 μmoL／L（Sco50组），测量各组LDH释放率，免疫组织化学法测定各组海马CA1区Bax、Bcl-2、Caspase-3的表达。结果PHC各组LDH释放率均较H／R组下降，以PHC50组效果最好（P〈0．01）。PHC50组Bcl-2阳性细胞的表达和Bcl-2／Bax比值均较H／R组升高，Bax和Caspase-3阳性细胞表达均较H／R组降低（P〈0．01）。Sco50组Bcl-2阳性细胞的表达和Bcl-2／Bax比值也较H／R组升高，Bax和Caspase-3阳性细胞表达均较H／R组降低（P〈0．01）。结论PHC可能通过减少LDH释放和Caspase-3、Bax的表达，增加Bcl-2的表达减轻大鼠缺氧缺糖／复氧复糖海马脑片的损伤。

Effect of penehyclidine hydrochloride on the expression of apoptosis-correlated factors in rat hippocampal slices in hypoxia/hypoglycemia and reoxygenation

Objective To investigate the protective effect of penehyclidine hydrochloride （PHC） on the apoptosis of rat hippocampal slices induced by hypoxia/hypoglycemia and reoxygenation （H/R） and the underlying mechanism. Methotis Experimental model of hypoxia/hypoglycemia and reoxygenation/glucose reintroduction was established by adoption of rat hippocampal slices, which were equally divided into 6 groups： Control group, H/R group, PHC 2 μmol · L^-1 （PHC2） group, PHC 10 μmol/L （ PHC10 ） group, PHC 50 μmol/L （ PHC50 ） group and Sco 50 μmol/L （ Sco50 ） group. The LDH release rate was used to evaluate the protective effect of PHC on the apoptosis of rat hippocampal slices induced by H/R. The expression of Bax, Bcl -2 and Caspase -3 in hippocampal CA1 field of each group were respectively detected by immunohistochemical method. Results Compared with H/R group, the LDH release rate in PHC groups decreased, with PHC50 group on the top ; the expression of Bcl - 2 positive cells and the Bcl - 2/Bax ratio in PHC50 group increased ; and the expression of Bax and Cspae - 3 positive cells decreased （ P 〈 0.01 ）. Compared with H/R group, the expression of Bcl - 2 positive ceils and the Bcl -2/Bax ratio in Sco50 group increased; and the expression of Bax and Cspae -3 positive cells decreased （P 〈0.01）. Conclusion PHC might attenuate the H/R -induced injuries to hippocampal slices by reducing the release rate of LDH, the expression of Caspase -3 as well as Bax and increase the expression of Bcl -2.