摘要
目的研究胡黄连苷Ⅱ对大鼠脑缺血再灌注损伤的神经保护作用。方法应用线栓法建立大鼠大脑中动脉闭塞再灌注(MCAO/R)模型,经尾静脉注射胡黄连苷Ⅱ(10mg/kg)和丹参素钠(10mg/kg)干预治疗,Bederson法评价动物的神经行为功能,氯化三苯基四氮唑(TTC)染色观察脑梗死体积,组织病理学观察神经细胞结构,原位缺口末端标记法(TUNEL)检测细胞凋亡。结果脑缺血再灌注损伤后,大鼠均表现神经行为功能障碍,缺血侧出现脑梗塞病灶,神经细胞凋亡数量均高于假手术组。胡黄连苷Ⅱ和丹参素钠治疗后,神经细胞凋亡数量明显减少、脑梗塞体积显著缩小,动物神经行为功能明显改善,与模型对照组比较均有显著性差异(P<0.05)。胡黄连苷Ⅱ组脑梗塞体积显著小于丹参素钠组(P<0.05)。结论胡黄连苷Ⅱ可能通过抑制细胞凋亡,缩小梗死体积而改善大鼠的神经行为功能。
Objective To investigate the neuroprotective effects of picrodide Ⅱ on cerebral ischemic reperfusion injury in rats. Methods Intraluminal thread methods were applied to establish the left middle cerebral artery occlusion reperfusion models （MCAO/R） in rats. Picrodide Ⅱ （10mg/kg） and salvianic acid A sodium （10mg/kg） were injected from tail vein for treatment. The neurological behavioral function was evaluated with Bederson＇s test. The cerebral infarction volume was observed with tetrazolium chloride （TTC） staining. The structure of ceils was observed with histopathology. The apoptosis positive cells were counted by terminal deoxynucleotidyl transferase midiated dUTP nick end labeling （TUNEL）. Results The neurological behavioral malfunction appeared in all rats with MCAO/R. The infarction focus showed in the ischemic hemisphere following cerebral ischemia reperfusion injury. In the picrodide Ⅱ and salvianic acid A sodium treatment groups, the number of apoptosis positive cells decreased and the cerebral infarction volume reduced, while the neurological behavioral function was significantly improved than those in the model control group （ P 〈 0.05 ）. The cerebral infarction volume in the picrodide Ⅱ group was smaller than that in the salvianic acid A sodium group （P 〈 0. 05）. Conclusion Picrodide Ⅱ might reduce cerebral infarction volume and improve the neurological behavioral function through inhibiting the neuronal apoptosis induced by ischemia reperfusion injury.
出处
《解剖学报》
CAS
CSCD
北大核心
2010年第1期9-12,共4页
Acta Anatomica Sinica
基金
国家自然科学基金资助项目(30873391)
