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目的:研究阿司匹林(aspirin,Asp)对脂多糖(lipopolysaccharide,LPS)诱导人主动脉内皮细胞(human aortic endothelial cells,HAECs)损伤的保护作用,并进一步阐明其对一氧化氮合酶(NOS)及血管内皮生长因子(VEGF)及其相关受体信号的调控。方法:LPS建立HAECs损伤模型。苏木精-伊红(HE)染色观察细胞形态;MTT法、划痕实验分析HAECs损伤修复能力;ELISA测定一氧化氮(NO)含量;Western blot检测内皮型一氧化氮合酶(eNOS)、诱导型一氧化氮合酶(iNOS)、VEGF和血管内皮生长因子受体-2(VEGFR-2)蛋白表达。结果 :给药12 h后Asp明显改善LPS(5 mg·L~(-1))导致的细胞损伤、提高修复能力(P<0.05),并上调NO分泌量及VEGF、VEGFR-2的蛋白表达(P<0.01);升高eNOS蛋白的表达(P<0.01)。而给药24 h后阿司匹林显著下调LPS导致的NO分泌量及iNOS、VEGF、VEGFR-2的蛋白表达升高,同时升高eNOS蛋白的表达(P<0.01)。结论:阿司匹林对LPS诱导的血管内皮细胞炎性损伤的保护作用与调节NOS/NO和VEGF及其受体的动态平衡密切相关。
Objective: To investigate the protective effect of aspirin (Asp) on the injury of human aortic endothelial cells (HAECs) induced by lipopolysaccharide (LPS), and to further investigate its protective effect on nitric oxide synthase (NOS) Regulation of Vascular Endothelial Growth Factor (VEGF) and Its Related Receptor Signaling. Methods: LPS established HAECs injury model. The morphology of the cells was observed by hematoxylin-eosin (HE) staining. The cell viability was detected by MTT assay and scratch assay. The content of nitric oxide (NO) was measured by ELISA. The expression of eNOS, INOS, VEGF and VEGFR-2 protein expression. RESULTS: Asp significantly improved the cell injury induced by LPS (5 mg · L -1) and improved the ability of repair (P <0.05) at 12 h after administration, as well as upregulated the secretion of NO and the protein expression of VEGF and VEGFR-2 (P <0.01), and increased eNOS protein expression (P <0.01). Aspirin down-regulated LPS-induced NO secretion and the expression of iNOS, VEGF and VEGFR-2, and increased the expression of eNOS protein (P <0.01). CONCLUSION: The protective effect of aspirin on LPS-induced inflammatory injury of vascular endothelial cells is closely related to the regulation of NOS / NO and the dynamic balance of VEGF and its receptor.