小檗碱对大鼠脑缺血再灌注后血清超氧化物歧化酶活性、丙二醛含量及神经功能的影响

目的观察小檗碱(BBR)对大鼠脑缺血再灌注损伤后超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量及神经功能的影响,探讨BBR在脑缺血再灌注损伤中的脑保护机制。方法将缺血再灌注模型大鼠随机分为模型组、BBR低剂量组(50 mg/(kg.d))、BBR高剂量组(150 mg/(kg.d))、假手术组,线栓法建立大鼠脑缺血再灌注损伤模型,脑缺血2 h再灌注24 h;分别在再灌注后2 h和24 h进行神经功能评分,并在再灌注12 h、24 h后断头取脑,检测BBR大鼠脑组织匀浆中SOD活性及MDA含量。结果 BBR组神经功能评分明显低于模型组。与假手术组相比,模型组MDA含量明显升高(P<0.01),SOD活性明显降低(P<0.01)。与模型组相比,BBR低剂量组和BBR高剂量组MDA显著降低,SOD活性升高,且高剂量组较低剂量组变化更明显(P<0.05)。结论 BBR能明显减轻脑缺血再灌注损伤所造成的行为障碍,能降低缺血再灌注大鼠SOD活性,升高MDA活性。BBR可能通过抑制氧化应激而减少细胞凋亡发挥脑保护作用。

Effect of Berberine on serum superoxide dismutase activity, MDA content and neural function in rats after cerebral ischemia reperfusion

Objective It is to observe the effect of berberine(BBR) on superoxide dismutase(SOD) activity,malondialdehyde(MDA) content and neural function in rats after cerebral ischemia-reperfusion injury,and to investigate the cerebral protection mechanism of BBR in cerebral ischemia-reperfusion injury.Methods The ischemia reperfusion model rats were randomly divided into model group,BBR low dose(50 mg/(kg·d))group,BBR high dose(150 mg/(kg·d))group,sham operation group.The models of cerebral ischemia-reperfusion injury were established by middle cerebral artery occlusion,cerebral ischemia for 2h and reperfusion for 24h.The scores of neurological behavior were evaluated at 2h and 24 h after reperfusion.The rats were put to death after 12h,24h reperfusion to get their brains to determine SOD activity and MDA effects.Results Compared to model group,the neural function scores were significantly lower in BBR group.Compared with sham operated group,the content of MDA was obviously increased(P<0.01) and activity of SOD was obviously decreased in model group(P<0.01).At the same time,the contents of MDA decreased(P<0.05),while the content of SOD in brain tissue increased(P<0.05) in BBR high dose group and BBR low dose group compared to model group,especially in high dose group(P<0.05).Conclusion BBR can obviously relieve the behavior disability induced by cerebral ischemia-reperfusion injury,it also can increase activity of SOD and decrease that of MDA,this brain protecting mechanism may be that it can inhibit oxidative stress to decrease cell apoptosis.