槲皮素对大鼠局灶性脑缺血再灌注损伤的保护作用

Protective effect of quercetin on focal cerebral ischemia-reperfusion injury in rats

目的探讨槲皮素对大鼠局灶性脑缺血再灌注损伤的保护作用及机制。方法将54只雄性SD大鼠随机分成三组:假手术组、缺血再灌注组、缺血再灌注+槲皮素组。采用线栓法制备大鼠大脑中动脉阻断局灶性脑缺血模型,缺血2 h,再灌注24 h;假手术组仅暴露左侧颈总动脉后缝合。缺血再灌注+槲皮素组大鼠在缺血30 min后腹腔注射槲皮素50 mg/kg,假手术组及缺血再灌注组大鼠按相同方式给予等体积溶剂。再灌注24 h后评价大鼠神经功能状态、脑组织含水量,观察脑组织形态学变化,制备脑组织匀浆并测定脑组织超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量。结果腹腔注射槲皮素后,大鼠神经功能评分降低、脑组织含水量下降、脑组织内SOD活性增加、MDA含量降低、脑组织损害减轻,差异有统计学意义(P<0.05)。结论槲皮素可通过调节抗氧化途径保护脑缺血再灌注引起的神经损伤。

Objective To investigate the protective effect and mechanism of quercetin on focal cerebral ischemia-reperfusion injury in rats.Methods A total of 54 male SD rats were randomly divided into 3 groups,which were the sham operation group,the ischemia-reperfusion group,and the ischemia-reperfusion plus quercetin group.The model of focal cerebral ischemia in rats with middle cerebral artery occlusion was made by suture method,and the model was ischemia for 2 h and reperfusion for 24 h.In the sham operation group,only common carotid artery was exposed and sutured.Rats in the ischemia-reperfusion plus quercetin group were injected with quercetin 50 mg/kg intraperitoneally after ischemia for 30 min,while rats in the sham operation group and the ischemia-reperfusion group were treated with the same volume of solvent in the same way.24 h after reperfusion,the neurological function and water content of brain tissue were evaluated,the morphological changes of brain tissue were observed,the homogenate of brain tissue was prepared,and the activity of superoxide dismutase(SOD)and the contents of malondialdehyde(MDA)in brain tissue were detected.Results After intraperitoneal injection of quercetin,the neurological function score of rats decreased,the water content of brain tissue descended,the activity of SOD in brain tissue increased,the content of MDA decreased and the damage of brain tissue alleviated,with statistically significant differences(P<0.05).Conclusion Quercetin can protect neurological injury caused by cerebral ischemia-reperfusion by regulating antioxidant pathway.