人参皂苷Rg1调控Nrf2在SD大鼠脑缺血再灌注损伤后的抗氧化作用

目的 探讨人参皂苷Rg1在大鼠脑缺血再灌注损伤中的抗氧化作用及机制.方法 SPF级健康成年雄性SD大鼠120只, 随机分为空白对照组、假手术组、模型组、不同浓度的Rg1治疗组.线栓法构建大鼠大脑中动脉栓塞 (middle cerebral artery occlusion, MCAO) 缺血再灌注损伤模型, 各治疗组采用人参皂苷Rg1进行预处理, 假手术组仅分离血管而不闭塞.采用Longa标准进行神经行为学评分;Western blot检测Nrf2和HO-1蛋白表达情况;比色法测定SOD和MDA含量变化.结果 模型组大鼠行为学评分显著高于空白对照组, 不同浓度的Rg1治疗组评分明显低于模型组 (P<0.05) ;与空白对照组或假手术组相比, 模型组Nrf2和HO-1的表达有所增加, SOD的含量显著降低, 而MDA的含量明显增加 (P<0.05) ;与模型组相比, 各治疗组Nrf2和HO-1的表达、SOD的含量均增加, 而MDA的含量则不同程度的减少 (P<0.05) .结论 人参皂苷Rg1上调Nrf2和HO-1蛋白表达, 增加SOD、降低MDA的含量, 改善SD大鼠脑缺血再灌注损伤后行为学表现, 发挥保护作用.

The Anti-antioxidant Role of Ginsenoside Rg1 Regulating Nrf2 on Focal Cerebral Ischemia Reperfusion SD Rats

Objective To study antioxidant role and mechanism of Rg1 in rats with cerebral ischemia reperfusion injury (IRI) .Me thods One hundred and twenty healthy male rats were randomly divided into six groups: control group, sham operation group, model group, different concentration (30, 60, 90 mg/kg) of Rg1 treatment group.MCAO SD rats model was established by suture-occluded method;the Rg1 treatment groups were given Rg1 i.p. in advance, after 24 hours of reperfusion, neurobehavioral scores of all groups were examined by Longa's standard;The expression of Nrf2 and HO-1 were analyzed by western blot;The content of SOD and MDA was detected by kit.Re s ults The score of model group rats are significantly higher than control group, compared with the model group, the score of different concentration of Rg1 treatment group was decreased (P<0.05) . The Nrf2 and HO-1 expression in model group was mildly higher than the control or sham group (P <0.05) . Both of them in every Rg1 treatment group was higher than model group. Compared with control or sham group, SOD content was observably depressed but MDA content was dramatically increased in model group, interestingly, SOD contentwas enhanced, MDA content was attenuated in different concentration of Rg1 treatment group (P <0.05) .Conclusion Rg1 increases Nrf2 and HO-1 protein expression and SOD content, reduces MDA content, improves neurofunctional performance of rats after MCAO, and alleviates cerebral cerebral IRI.