摘要
目的：研究东菱克栓酶是否通过影响热休克蛋白７０（ＨＳＰ７０）起神经保护作用。方法：采用大鼠大脑中动脉线栓法缺血再灌注模型，以免疫细胞化学及病理形态学方法进行研究。结果：发现在缺血（９０ｍｉｎ）再灌注（４８ｈ）后，对照组缺血侧皮层ＨＳＰ７０免疫反应增强及皮层神经细胞有缺血性损伤，在缺血９０ｍｉｎ后给予东菱克栓酶（８ＢＵ／ｋｇ）者，则在再灌注４８ｈ后，ＨＳＰ７０免疫反应较对照组更强烈，而皮层神经元缺血性损伤则较轻。结论：东菱克栓酶对局灶性缺血再灌注损伤的神经保护作用，可能与它能影响热休克蛋白有关。
OBJECTIVE:To investigate the effect of batroxobin on the heat shock protein 70 (HSP70)expression in cerebral focal ischemic reperfusion rats.METHODS:A middle cerebral artery(MCA)thread embolism rat model and immunocytochemistry method were used.RESULTS:Immunoreactive staining for antiHSP70 was only slightly detected in cortical neurons of shamoperated animals,strong staining was detected in controls after 90 min ischemia followed by 48 h reperfusion.When rats treated with batroxobin shortly after 90 min ischmia,the staining of cortical neurons was much stronger than that of control rats.Batroxobintreated rats had less neuronal damage in the cortex than control ones.CONCLUSION:The results suggest that batroxobin affords protection against ischemic reperfusion injury by the induction of HSP70.
出处
《中国新药杂志》
CAS
CSCD
1998年第1期56-58,共3页
Chinese Journal of New Drugs
