巴曲酶的神经保护作用—缺血再灌注后不同时程热休克蛋白70及病理组织学变化的相关性研究

Neuroprotective effect of batroxobin on heat shock protein 70 after focal ischemic reperfusion time course evaluated by immunocytochem Istry analysis and histopathology

本文研究目的为巴曲酶是否影响热休克蛋白起到神经保护作用。用中大脑动脉(MCA)线栓法缺血再灌注大鼠模型。Wistar大鼠共51只。发现:在再灌注1h、2h、3h对照组与巴曲酶组(8BU/kg ip)HSP70均呈轻度表达,从再灌注12h起表达显著,至再灌注后24h达高峰,至再灌注后6d仅见于坏死灶周围,至再灌注后14d恢复至假手术组水平。巴曲酶组的HSP70表达变化在时程上与对照组一致,但在再灌注12h起至6d较对照组显著,同时相应时间点的MCA血供区皮层神经细胞有缺血变性者巴曲酶组少而轻。本文结果提示巴曲酶的神经保护作用,可能与它能影响HSP70蛋白合成的调控机制有关。

In this study, 45 Wistar Rats were divided into three groups, sham - operated(n=3),control group(n = 21),Batroxobin group (n = 21). Batroxobin was examined for its effect on HSP 70 induction in rat cerebral cortex at various recir-culation levels after 90min ischemia using middle cerebral vessel thread occlusion rat model. In immunocytochemical analysis using anti-HSP70 antibody,in control group a little induction of HSP 70 appeared after 90min ischemia followed by Ih reperfusion and reached a maximum level at 48h. In atninals treated with batroxobin 90 min after ischemia,the time course of HSP 70 induction after recirculation was same as the control animals,The results suggest that HSP 70may play an important role in the neuroprotective mechanism of batroxobin in cerebral ischemic reperfusion injury.