中文摘要：

目的：通过建立氧糖剥夺再灌注模型,观察补阳还五汤对氧糖剥夺再灌注诱导脑微血管内皮细胞（r BMECs）氧化应激损伤的作用,并进一步探讨沉默调节蛋白1（Sirtuin type 1,SIRT1）是否是其发挥作用的靶点。方法：分离培养原代大鼠脑微血管内皮细胞,建立体外氧糖剥夺再灌注损伤模型,SD大鼠按15g/kg的剂量每日灌胃给药补阳还五汤1次,连续灌胃1周后分离得到血清,将细胞分为尼莫地平组、对照组、模型组、补阳还五汤含药血清低剂量组（10%）,补阳还五汤含药血清高剂量组（20%）,应用CCK-8法检测细胞存活率,测定补阳还五汤含药血清对r BMECs活力的影响,检测细胞中乳酸脱氢酶（LDH）、丙二醛（MDA）及活性氧簇（ROS）含量,并采用Western blot、实时荧光定量聚合酶链式反应（q PCR）检测SIRT1表达水平。结果：与对照组相比,氧糖剥夺再灌注处理组的细胞存活率明显降低,LDH活性及ROS、MDA的含量升高,SIRT1蛋白、m RNA表达明显下降;与损伤组相比,10%、20%的补阳还五汤含药血清能明显提高氧糖剥夺再灌注损伤后细胞的存活率,降低LDH、ROS、MDA的含量,提高SIRT1蛋白、m RNA的表达;尼莫地平组与补阳还五汤高低剂量组差异无显著。结论：补阳还五汤对脑微血管内皮细胞氧糖剥夺再灌注诱导的氧化应激损伤具有明显的保护作用,其作用机制可能是通过上调SIRT1表达水平实现的。

英文摘要：

Objective： To establish an oxygen-glucose deprivation and reperfusion（OGD/R） model, and to investigate the effect and the possible mechanism of serum containing Buyang Huanwu Decoction against oxidative stress injury of rBMECs induced by oxygen and glucose depriva- tion-reperfusion injury. Methods： The in vitro oxygen and glucose deprivation-reperfusion injury model was established by culturing the isola- ted primary rat brain mierovascular endothelial cells. SD rats were treated with Buyang Huanwu Decoction once a day at a dose of 15 g / kg, and serum was isolated after one week of continuous gavage. The cells were divided into four groups, namely control group, oxygen and glucose deprivation-reperfusion group, 10% Buyang Huanwu decoction containing serum group and 20% Buyang Huanwu decoction containing ser- um, then were processed by follow/ng steps. Cell counting kit-8 （CCK-8） method was used to detect cell activity. The activity of lactate dehy- drogenase（LDH） and oxygen species （ROS）,the content of malondialdehyde （MDA） in the medium were determined. Western blot assay was used to detect protein expressions of SIRT1. Real-time fluorescent quantitative PCR （qPCR） was used to detect the mRNA expressions of SIRT1. Results： Incubation of rBMECs with different concentrations of the serum containing Buyang Huanwu decoction （ 10%, 20% ） en- hanced cell viability. Compared with the model group, 10%, 20% serum containing Buyang Huanwu decoction which pretreated with cells decreased levels of LDH, ROS, MDA, up-regulated the expressions of SIRT1 protein and mRNA, and no difference was discovered in the rats among nimodipine group and buyanghuanwu decoction groups （ P 〉 0. 05 ）. Conclusion： This study results suggest that baicalin could in- hibit the oxygen-glucose deprivation and reperfusion-induced oxidative stress injury. The further mechanism study shows that Buyang Huanwu decoction can inhibit oxidative stress injury via up-regulating SIRT1.