中文摘要：

目的：研究藁本内酯对糖氧剥夺-复糖氧损伤血管内皮细胞活性及NO/NOS与HIF-1α、VEGF、Tubulin表达的影响。方法：将融合生长的人脐静脉血管内皮细胞（HUVEC）预处理给予藁本内酯1h后,用连二亚硫酸钠（Na2S2O4）制备糖氧剥夺-复糖氧损伤（oxygen-glucose deprivation-reperfusion injury,OGD-R）模型,采用MTT法检测细胞活性,微板法检测细胞内丙二醛（MDA）、细胞外一氧化氮（NO）含量与测定细胞内一氧化氮合酶（NOS）活性,WTS-1法测定细胞内超氧化物歧化酶（SOD）活性;采用高内涵分析系统检测缺氧诱导因子-1α（HIF-1α）、血管内皮生长因子（VEGF）的表达,采用蛋白免疫印迹法测定细胞内微管蛋白Tubulin的表达。结果：与溶剂对照组比较,OGD-R损伤的HUVEC细胞活力明显下降,细胞内MDA含量增加而SOD活性降低、细胞外NO含量与细胞内NOS活性均下降,细胞内HIF-1α、VEGF和Tubulin表达明显上升;藁本内酯20、40、60μmol/L可提高OGD-R损伤的HUVEC的活力,降低细胞内MDA含量和提高SOD活性,同时增加细胞外NO含量与细胞内NOS活性,提高细胞内HIF-1α、VEGF的表达和Tubulin的含量。结论：藁本内酯预处理对OGD-R损伤的HUVEC有保护作用,可对抗细胞氧化损伤,并调节内皮细胞功能。

英文摘要：

Obiective： To observe the expression of HIF-1α,VEGF,Tubulin in vascular endothelial cell pretreated with Ligustilide（ LIG） after oxygen-glucose deprivation-reperfusion（ OGD-R） injury. Methods： Human umbilical vein endothelial cells（ HUVEC） were involved in the experiment. When fusion growth,cells were grouped into solvent control（ with 0. 1% methyl alcohol pretreated）,treatment groups（ with 20,40,60μM of LIG pretreated,respectively） and model group（ with 0. 1% methyl alcohol pretreated）. After received drug intervention for1 h,ischemia-reperfusion injury models were established by sodium dithionite for every group except solvent control. Cell viability was measured by MTT colorimetric method,intracellular Malondialdéhyde（ MDA）,NO content and the activity of NOS and SOD were measured by kits. The expression of HIF-1α and VEGF were detected by high-content screening（ HCS） and analysis system. Tubulin were determined by western blot and analyzed by Quantity One. Results： Cell viability,the content of NO and the activity of NOS and SOD were decreased after OGD-R injury,while MDA content,HIF-1α,VEGF and Tubulin expression in cells were increased. LIG at the concentration of 20-60μM enhanced cell viability,promoted the content of NO and the activity of NOS and SOD against OGD-R injury and lower MDA content in cells.HCS showed that LIG promoted the OGD-R injury-induced HIF-1α and VEGF expression. LIG promoted the OGD-R injury-induced Tubulin expression as well,according to western blot. Conclusions： LIG protect against OGD-R injury-induced HUVEC damage,resistance to oxidation damage and regulating cell function ability.