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作 者:何晓乐[1] 王晓明[1] 葛伟[1] 李榕[1] 王琳[1] 王宁[1] 许荣[1] 贾新[1] 刘军[1,2]
机构地区:[1]第四军医大学西京医院老年病科,西安710032 [2]兰州军区总兰州医院全军骨科研究所,兰州730000
出 处:《中华老年多器官疾病杂志》2017年第3期203-207,共5页Chinese Journal of Multiple Organ Diseases in the Elderly
基 金:国家自然科学基金(81370927);陕西省自然科学基金(2013JM4009);甘肃省青年科技基金(1606RJYA300)~~
摘 要:目的观察姜黄素(Cur)对内脂素(visfatin)诱导的人脐静脉内皮细胞(HUVECs)炎症损伤过程的影响,探讨Cur改善内皮功能的信号传导机制。方法将HUVECs随机分组,根据前期实验结果,给予1×10^(-5)mol/L的visfatin进行诱导,加入Cur后MTT法检测内皮细胞活力变化。通过酶联免疫吸附法(ELISA)检测单核细胞趋化蛋白-1(MCP-1)、E选择素(E-selectin)的含量变化,蛋白质印迹法(Western blotting)检测细胞黏附分子-1(ICAM-1)、需肌醇激酶/核酸内切酶1(IRE1)、葡萄糖调节蛋白78(GRP78)的表达。结果 MTT检测结果表明,正常HUVECs加入Cur后,不影响内皮细胞活力;而与正常对照组相比,给予1×10^(-5)mol/L visfatin处理后,MCP-1和E-selectin含量明显增加,ICAM-1、IRE1及GRP78的表达增加,差异有统计学意义(P<0.05)。与visfatin组相比,给予不同浓度Cur处理后,可显著降低MCP-1和E-selectin的含量,同时ICAM-1、IRE1及GRP78的表达也显著降低,差异有统计学意义(P<0.05)。结论Cur可能通过抑制内质网应激(ESR)来拮抗visfatin诱导HUVECs炎症损伤。Objective To determine the effect of curcumin ( Cur) on the process of visfatin-induced injury in human umbilical vein endothelial cells (HUVECs), and investigate the underlying mechanism of signal pathway induced by Cur treatment in the improvement of endothelial functions .Methods After the HUVECs were induced by 1 ×10^-5 mol/L visfatin, the cells were treated by Cur .Then cell viability was determined by MTT assay , the expression levels of monocyte chemoattractant protein-1 ( MCP-1) and E-selectin were detected by enzyme linked immunosorbent assay (ELISA), and the levels of intercellular cell adhesion molecule-1 (ICAM-1), inositol-requiring transmembrane kinase/endonuclease 1 (IRE1), glucose-regulated protein 78 (GRP78) were measured by Western blotting. Results MTT assay showed that Cur treatment had no effect on cell viability .Compared with the normal control group , 1 ×10 ^-5 mol/L visfatin significantly increased the protein expression levels of MCP-1 and E-selectin (P〈0.05), and obviously enhanced the protein expression of ICAM-1, IRE1 and GRP78 (P〈0.05).However, different doses of Cur treatment exerted inhibitory effects on the above phenomena induced by visfatin (P〈0.05).Conclusion Cur may mitigate visfatin-induced injury in HUVECs via the inhibition of endoplasmic reticulum stress.
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