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目的研究牡荆苷对脑缺血再灌注损伤小鼠抗氧化酶的作用及机制。方法雄性昆明种小鼠70只,按随机数字表法分为正常对照组、假手术组、模型组、牡荆苷组(10、20、40 mg/kg)、尼莫地平组(0.6 mg/kg),采用线栓法制备脑缺血再灌注模型,牡荆苷组在缺血再灌注前连续腹腔给予牡荆苷3 d,缺血再灌注后,每天给药1次,连续给药7 d,检测小鼠神经功能损伤评分,采用试剂盒法检测脑组织、血清中丙二醛(MDA)含量、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)、髓过氧化物酶(MPO)的活性。结果与假手术组比较,模型组神经功能损伤评分显著升高(P<0.01);与模型组比较,牡荆苷组神经功能损伤评分显著降低(P<0.01)。与假手术组比较,模型组脑组织、血清中MDA含量、MPO活性显著升高,SOD、GSH-Px、CAT活性显著降低,差异均有高度统计学意义(P<0.01);与模型组比较,尼莫地平组和牡荆苷组脑组织、血清中MDA含量、MPO活性显著降低,SOD、GSH-Px、CAT活性显著增强,差异有统计学意义(P<0.01或P<0.05)。与尼莫地平组比较,10、20 mg/kg牡荆苷组MDA含量和MPO活性显著上升,SOD、GSH-Px、CAT活性显著降低(P<0.05);40 mg/kg牡荆苷组与尼莫地平组比较差异无统计学意义(P>0.05)。结论牡荆苷对小鼠脑缺血再灌注损伤的保护作用可能通过抗氧化作用来实现。
Objective To study the effect and mechanism of vitexin on antioxidant enzyme in mice with cerebral ischemia-reperfusion injury. Methods Seventy male Kunming mice were randomly divided into normal control group, sham operation group, model group, vitexin group (10,20,40 mg / kg), nimodipine group (0.6 mg / kg). Cerebral ischemia-reperfusion model was established by thread embolization. Vitexin group was given intraperitoneal vasopressin for 3 days before ischemia-reperfusion. After ischemia-reperfusion, the model was administered once daily for 7 consecutive days The neurological impairment scores of mice were detected. The contents of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione Oxidase (GSH-Px), myeloperoxidase (MPO) activity. Results Compared with the sham-operation group, the score of neurological impairment in the model group was significantly increased (P <0.01). Compared with the model group, the score of neurological impairment in the vitexin group was significantly decreased (P <0.01). Compared with sham operation group, MDA content, MPO activity and SOD, GSH-Px and CAT activities in brain tissue and serum of model group were significantly decreased (P <0.01), compared with model group , Nimodipine group and vitexin group, MDA content, MPO activity, SOD, GSH-Px and CAT activity in brain tissue and serum were significantly decreased (P <0.01 or P <0.05). Compared with the nimodipine group, the content of MDA and the activity of MPO in 10,20 mg / kg vitexin group increased significantly (P <0.05), and the activity of SOD, GSH-Px and CAT decreased significantly There was no significant difference in nimodipine group (P> 0.05). Conclusion The protective effect of vitexin on cerebral ischemia-reperfusion injury in mice may be through the anti-oxidative effect.