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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。
AIM: To investigate the effects of ligustilide on the activity of vascular endothelial cells and the expression of NO / NOS, HIF-1α, VEGF and Tubulin induced by glucose-oxygen deprivation-polysaccharide oxygen. Methods: HUVECs were pretreated with ligustilide for 1 h and then treated with sodium dithionite (Na2S2O4) to prepare oxygen-glucose deprivation-reperfusion injury (HUVEC) OGD-R) model was established. Cell viability was measured by MTT assay. Malondialdehyde (MDA), extracellular nitric oxide (NO) and intracellular nitric oxide synthase (NOS) -1 was used to measure the activity of superoxide dismutase (SOD). The expression of hypoxia inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) was detected by high content analysis system. Expression of intracellular tubulin Tubulin. RESULTS: Compared with the solvent control group, the viability of HUVECs with OGD-R injury was significantly decreased. The intracellular MDA content was increased while the SOD activity was decreased. The content of NO and intracellular NOS activity were decreased. The expression of HIF-1α, VEGF and Tubulin L by ligustilide 20, 40 and 60μmol / L increased the activity of OGD-R-injured HUVECs, decreased intracellular MDA content and increased the activity of SOD, increased the content of extracellular NO and intracellular NOS activity, Expression of HIF-1α, VEGF and Tubulin in HUVECs. Conclusion: ligustilide preconditioning can protect OECs against HUVEC injury induced by OGD-R and protect against oxidative damage and endothelial function.