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丙泊酚对大鼠局灶性脑缺血-再灌注时脑组织热休克蛋白70基因和蛋白表达的影响 被引量:4

Effects of propofol on expression of HSP70 mRNA and HSP70 in cerebral cortex during transient focal cerebral ischemia-reperfusion in rats
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摘要 目的观察丙泊酚对大鼠局灶性脑缺血-再灌注时脑组织热休克蛋白(HSP)70 mRNA和HSP70蛋白表达的影响,以探讨其脑保护的机制。方法采用大脑中动脉线栓法建立大鼠局灶性脑缺血-再灌注模型。60只雄性Wistar大鼠,随机分为假手术组(Sham组)、缺血-再灌注组(I-R组)和丙泊酚组(P组),每组20只。大鼠脑缺血2 h,然后进行再灌注。在再灌注3、6、24、72 h断头取脑组织,采用原位杂交法和免疫组织化学染色检测大鼠脑组织HSP70 mRNA和HSP70蛋白的表达。结果局灶性脑缺血-再灌注后,HSP70 mRNA和HSP70蛋白的表达增加(P<0.01),但HSP70 mRNA表达较早,分布范围较广泛,而HSP70蛋白表达以半暗带区为主。应用丙泊酚能显著地促进脑缺血-再灌注后脑组织中HSP70 mRNA和HSP70蛋白的表达(P<0.01),与脑缺血-再灌注组相比较,HSP70 mRNA和HSP70蛋白不仅表达增多、范围增加,而且还能延缓下降(P<0.05)。结论丙泊酚能促进大鼠局灶性脑缺血-再灌注时HSP70的表达,这可能是其脑保护作用的部分机制。 Objective To investigate the effects of propofol on expression of HSP70 mRNA and HSP70 in the cerebral cortex during transient focal cerebral ischemia-reperfusion in rats. Methods The focal cerebral ischemia-reperfusion model was established by thread embolism of middle cerebral artery. Sixty adult male Wistar rats were randomly allocated to sham operation group (Sham) ,ischemia-reperfusion group (I-R) and propofol group with 20 animals each. Rats were subjected to 2 hours of focal ischemia by left middle cerebral artery occlusion (MCAO) and then reperfused. At 3,6,24 and 72 hours after reperfusion, the rats were decapitated,the expression of HSP70mRNA and HSP70 in ischemic versus nonischemic cortex were examined using in situ hybridization and immunohistochemistry method. Results The expression of HSP70 mRNA and HSP70 in ischemic cortex increased significantly at different time points after focal cerebral ischemia-reperfusion (P〈0.01). The expres sion of HSP70mRNA appeared early and had a wide distribution in ischemic cerebral hemisphere. Whereas, the expression of HSP70 focused in ischemic penumbra. Intraperitoneal injection of propofol ( 100 mg/kg) significantly enhanced the expression both of HSP70 mRNA and HSP70 in ischemic cortex (P〈0.01),increased width of their expression and prolonged their expression time during focal cerebral ischemia-reperfusion at different time points as compared with that of ischemia-reperfusion group (P〈0. 05). Conclusion This study demonstrates that propofol enhances the expression of HSP70 mRNA and HSP70 during focal cerebral ischemia-reperfusion, which may be one of the mechanisms of its neuroprotection.
出处 《临床麻醉学杂志》 CAS CSCD 2006年第3期207-210,共4页 Journal of Clinical Anesthesiology
关键词 丙泊酚 脑缺血 再灌注损伤 热休克蛋白 Propofol Cerebral ischemia Reperfusion injury Heat shock protein
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