摘要
目的进一步探讨蕲蛇酶对大鼠脑缺血再灌注损伤的保护作用及其机制。方法采用线栓法制备大鼠大脑中动脉闭塞后再灌注(MCAOR)模型,观察大鼠MCAOR时神经功能状态,同时,TTC染色测脑梗死面积,电镜观察脑血管超微结构,放免法测定血浆血栓素B2及6-酮前列腺素F1α含量。用药组分别在缺血即刻或再灌注即刻静脉给药,观察比较模型组和蕲蛇酶所有给药组之间上述指标的变化。结果蕲蛇酶所有给药组都能有效改善MCAOR大鼠神经功能缺失症状,明显减小梗死灶,调节血栓素B2/6-酮前列腺素F1α,保护血管内皮细胞,维持微血管正常结构。结论蕲蛇酶对脑缺血再灌注损伤保护作用可能与维持血栓素B2/6-酮前列腺素F1α平衡、改善脑微循环有关。
Aim To further study the protecnve effects of acutobin on focal cerebral ischemia -reperfusion injury in rats. Methods Reversible middle cerebral artery occlusion （MCAO） models were produced by intraluminal suture technique, and reperfusion was begun 3 hours after occlusion and lasted 24 h. The extent of neurological deficits was evaluated by Longa＇ method; The cerebrovascular morphology was observed by electron microscope. The infarct area of brain was measured by 2,3,5-triphenyltetrazolium chloride （TTC） staining technique;The 2 -4 U·kg^-1 doses of Acutobin were administrated i.v. at the beginning of ischemia or reperfusion respectively. Results ① After 3-h occlusion and 24 h reperfusion, the neurological syndromes and the infarct area were showed, the change of cerebrovascular morphology were appeared and the ratio of TXB2/6-Keto-PGF1α, in plasma was increased. ② After different doses of acutobin were administrated at different time respectively, the neurological syndromes were alleviated; the infarct areas of brain were diminished; the hurt of cerebrovascular endothelial cell was lessened and the ratios of TXB2/6-Keto-PGF1α in plasma were reduced. Conclusion Protective effects of acutobin on cerebral ischemia-reperfusion injury in rats may be related to lessening cerebrovascular injury and balancing the ratio of TXB2/6-Keto-PGF1α.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2005年第9期1100-1103,共4页
Chinese Pharmacological Bulletin
基金
福建省自然科学基金资助项目(NoC0010012和NoC021009)
