摘要
目的观察丙酮酸乙酯对大鼠全脑缺血再灌注损伤海马CA1区细胞凋亡及凋亡调控基因Bcl-2、Bax表达的影响,为进一步的研究提供依据。方法本实验采用二血管阻断加低血压法制备大鼠全脑缺血再灌注模型。SD大鼠24只,随机被分成3组,每组8只:①假手术组(F组):只分离股动脉和双侧颈总动脉,不降压,不夹闭双侧颈总动脉;②缺血再灌注组(IR组):股动脉放血使血压降至基础血压的50%～60%,夹闭双侧颈总动脉10min再放开;③丙酮酸乙酯处理组(EP组):与IR组处理相同。EP组于恢复血流即刻腹腔注射丙酮酸乙酯40mg/kg,其余两组给予等量生理盐水,每隔6h注射一次;再灌注24h后断头取脑,用原位末端转移酶标记(TUNEL)法检测细胞凋亡指数(AI),免疫组化法检测海马CA1区Bax、Bcl-2蛋白的表达。结果IR组和EP组AI和Bcl-2、Bax蛋白表达水平均明显高于F组,差异有统计学意义(P<0.05);与IR组比较,EP组AI显著降低、Bax蛋白表达水平显著下降以及Bcl-2蛋白表达水平显著升高,差异有统计学意义(P<0.05)。结论丙酮酸乙酯可抑制大鼠全脑缺血再灌注损伤细胞凋亡,此作用可能与其减轻氧化应激、上调Bcl-2和下调Bax表达水平有关。
Objective To observe the effects of ethyl pyruvate on apoptosis and expressions of Bcl - 2 and Bax in hippocampal CA1 regions in rats with global cerebral ischemia reperfusion injury. Methods The model of global cerebral ischemia - reperfusion injury was used in this study. Twenty- four male Sprague -Dawley （SD） rats were randomly divided into control group, ischemia reperfusion group and ethyl pyruvate treatment group with 8 rats in each group. Femoral artery and bilaterial common carotid arteries were exposed in control group （ F group）. The blood pressure was lowered to 50% - 60% of the base value by bloodletting and the bilateral common carotid arteries underwent transient occlusion for 10 min in ischemia reperfusion group（ IR group）. 40 mg/kg of ethyl puruvate was immediately administered by intraperitoneal injection after ischemia -reperfusion and repeated every 6 hours in ethyl pyruvate treatment group （EP group）. 24 hours later, the rats were sacrificed and hippocampal CA1 regions were isolated for the test of brain apoptotic index （AI） by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling （TUNEL） assay, Bax and Bcl -2 proteins were detected by immunohistochemistry. Results Compared with F group, the AI and the expressions of Bcl - 2 and Bax proteins were increased in IR group and EP group （ P 〈 0.05 ） ; Compared with IR group, the AI and the expression of Bax protein were decreased obviously and the expression of Bcl - 2 protein was upregulated in EP group （ P 〈 0. 05 ）. Conclusion Ethyl pyruvate alleviates cerebral ischemia - reperfusion injury via inhibiting cell apoptosis and the mechanism may relate to upregulation of Bcl - 2 protein and downregulation of Bax protein.
出处
《临床和实验医学杂志》
2009年第8期1-2,5,共3页
Journal of Clinical and Experimental Medicine
基金
广西自然科学基金项目(NO:桂科自0640091)
