CAJ | 학술논문

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.
목적 연구호황련감Ⅱ대대서뇌결혈재관주손상적신경보호작용.방법 응용선전법건립대서대뇌중동맥폐새재관주(MCAO/R)모형,경미정맥주사호황련감Ⅱ(10mg/kg) 화단삼소납(10mg/kg)간예치료,Bederson법평개동물적신경행위공능,록화삼분기사담서(TTC)염색관찰뇌경사체적,조직병이학관찰신경세포결구,원위결구말단표기법(TUNEL)검측세포조망.결과 뇌결혈재관주손상후,대서균표현신경행위공능장애,결혈측출현뇌경새병조,신경세포조망수량균고우가수술조.호황련감Ⅱ화단삼소납치료후,신경세포조망수량명현감소、뇌경새체적현저축소,동물신경행위공능명현개선,여모형대조조비교균유현저성차이(P<0.05).호황련감Ⅱ조뇌경새체적현저소우단삼소납조(P<0.05).결론 호황련감Ⅱ가능통과억제세포조망,축소경사체적이개선대서적신경행위공능.
Objective To investigate the neuroprotective effects of picrodideⅡ 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. PicrodideⅡ (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 cells 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 picrodideⅡ 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 picrodideⅡ group was smaller than that in the salvianic acid A sodium group (P<0.05).Conclusion PicrodideⅡ might reduce cerebral infarction volume and improve the neurological behavioral function through inhibiting the neuronal apoptosis induced by ischemia reperfusion injury.