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目的:探讨蛇床子素对低密度脂蛋白诱导的人脐静脉血管内皮细胞(HUVEC)凋亡的影响及其机制研究。方法:采用HUVEC细胞,设置正常组、模型组和给药组,细胞培养12 h后,低密度脂蛋白进行细胞损伤,同时给予不同浓度蛇床子素(10、20、40μmol/L)进行干预,应用MTT法检测细胞活力;Annexin V-FITC标记的流式细胞术检测细胞凋亡;检测一氧化氮生成量;免疫印迹法检测p-AKt和p-eN OS蛋白表达水平。结果:与正常组相比,模型组细胞活力和凋亡率有显著差异;与模型组相比,蛇床子素提高细胞活力,抑制细胞细胞凋亡,作用效果呈剂量依赖性,20、40μmol/L蛇床子素均有显著性差异;与模型组相比,20、40μmol/L蛇床子素显著促进细胞一氧化氮合成;蛋白质检测结果显示,与模型组相比,蛇床子素可上调HUVEC细胞中Akt和eN OS蛋白磷酸化水平。结论:蛇床子素能够抑制ox-LDL诱导HUVEC的凋亡而发挥其保护作用,其作用机制可能与其激活Akt/eNOS/NO的信号通路相关。
Objective: To investigate the effects of osthole on the apoptosis of human umbilical vein endothelial cells (HUVEC) induced by low density lipoprotein and its mechanism. Methods: HUVEC cells were used to establish normal group, model group and administration group. Cells were cultured for 12 h. Low density lipoprotein (LDL) was used to induce cell injury. At the same time, different doses of osthole (10, 20 and 40 μmol / L) Cell viability was detected by MTT assay. Apoptosis was detected by flow cytometry with Annexin V-FITC assay. Nitric oxide production was measured by Western blotting. Expression of p-Akt and p-eNOS were detected by Western blotting. Results: Compared with the normal group, the viability and apoptosis rate of the model group were significantly different. Compared with the model group, osthorin increased the cell viability and inhibited the apoptosis of the cells in a dose-dependent manner. 20,40 μmol / L osthole were significantly different; compared with the model group, 20, 40μmol / L Osthole significantly promoted cell nitric oxide synthesis; protein test results showed that compared with the model group, osthole can up-regulate HUVEC cells Phosphorylation levels of Akt and eNOS proteins. Conclusion Osthole can inhibit the apoptosis of HUVEC induced by ox-LDL and exert its protective effect. Its mechanism may be related to its activation of Akt / eNOS / NO signaling pathway.