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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。
The purpose of this study is whether batroxobin can affect neuroprotective effect of heat shock protein. Rat model of ischemia - reperfusion induced by middle cerebral artery occlusion (MCA). A total of 51 Wistar rats. The results showed that the expression of HSP70 in the control group and the batroxobin group (8BU / kg ip) at 1h, 2h and 3h after reperfusion was mildly mild and reached a peak at 12h after reperfusion, reached the peak at 24h after reperfusion, 6d only seen around the necrotic lesions, 14d after reperfusion to return to sham group level. The change of HSP70 expression in Batroxobin group was consistent with the control group on the time course, but significantly increased from 12h to 6d after reperfusion, and at the same time MCA blood donor cortical neurons had ischemic degeneration Batroxobin Group less and light. Our results suggest that batroxobin neuroprotective effect may be related to its regulation of HSP70 protein synthesis mechanism.