中文摘要：

目的研究紫杉醇对脑缺血一再灌注（I-R）后海马神经元损伤的保护作用及分子机制。方法SD大鼠随机分为假手术对照组（A组）、I-R对照组（B组）、1％DMSO溶剂处理组（C组）、紫杉醇8μg／kg组（D组，缺血前30min脑室注射），每组各10只。采用大鼠四动脉结扎全脑缺血模型，应用免疫印迹法检测紫杉醇对B细胞淋巴瘤-白血病2（Bcl-2）、半胱天冬氨酸蛋白酶3（Caspase-3）表达的影响。结果与A组相比，B、c组Bcl-2及Caspase-3磷酸化表达增J／l（P〈0．05），而D组BcF2及Caspase-3磷酸化表达较B组明显减少（P〈O．05）。结论紫杉醇可能对脑I-R诱导海马神经元的损伤有保护作用；这种保护作用可能与Bcl-2、Caspase-3蛋白活性密切相关。

英文摘要：

Objective To investigate the effect and molecular mechanism of paclitaxel on the injury of hippocampal neurons induced by cerebral ischemiareperfusion（I-R）. Methods SD rats were randomly divided into four groups of A（sham operation）, B（I-R model）, C（injection of 1 % DMSO） and D（intraventricular injection of paclitaxel 8 μg/kg 30 rnin before ischemia） with 10 rats each. The cerebral ischemia model was established by fourvessel occlusion, and the expressions of B cell lymphoma/leukemia-2（Bcl-2） and cystein asparate proteinase-3（Caspase-3） were detected by Western blot. Results Compared with group A, the phosphorylation of Bcl-2 and Caspase-3 was increased in groups of B and C（P〈0. 05）. However, the phosphorylation of Bcl-2 and Caspase-3 in group D was significantly lower than that in group B（P〈0. 05）. Conclusion Paclitaxel may protect I-R-induced injury of hippocampal neurons, which is probably related with the activation of Bcl-2 and Caspase-3.