基于TRPV1受体研究吴茱萸碱对脂多糖诱导血管内皮细胞损伤的保护作用  

Research of Evodiamine in improving inflammatory injury of Human umbilical vein endothelial cells induced by lipopolysaccharide through transient receptor potential vanilloid 1 receptor

作　　者：王嫣 杨卫平 彭芳 陈天琪 付云燕 田敏 WANG Yan;YANG Wei-ping;PENG Fang;CHEN Tian-qi;FU Yun-yan;TIAN Min(Guizhou University of Traditional Chinese Medicine,Guiyang,Guizhou,550025,China)

机构地区：[1]贵州中医药大学,贵州贵阳550025

出　　处：《时珍国医国药》2020年第12期2897-2899,共3页Lishizhen Medicine and Materia Medica Research

基　　金：国家自然科学基金(81903840);贵州省中医药管理局中医药、民族医药科学技术研究课题(QZYY2017-006)。

摘　　要：目的观察吴茱萸碱对脂多糖(LPS)诱导人脐静脉内皮细胞(HUVECs)损伤的干预作用,探讨其可能的作用机制。方法用HUVECs制备细胞炎症损伤模型,分为正常对照组、LPS模型组、DMSO对照组、吴茱萸低、高剂量组、CAPZ组。采用CCK-8法检测细胞的增殖能力,Elisa检测培养液上清中NO的含量,Western-blot检测各组细胞中TLR4、NF-κB p65的蛋白表达。结果与正常对照组相比,LPS模型组细胞的增殖能力显著降低,培养液中NO的含量显著降低,TLR4、NF-κB p65蛋白表达均明显增加。用吴茱萸碱预处理后,与模型组相比,细胞的增殖能力明显提高,培养液中NO的含量明显增加,同时细胞中TLR4、NF-κB p65蛋白的表达受到抑制。在加入TRPV1受体阻断剂后,与吴茱萸碱高剂量组相比,细胞的增殖数量降低,NF-κB p65蛋白表达增加,提示吴茱萸碱的作用受到抑制。结论吴茱萸碱可能通过TRPV1受体抑制TLR4/NF-κB通路,促进细胞的增殖和NO的合成,从而减轻LPS所致的内皮细胞炎性损伤。Objective To observe the effect of evodiamine on injured human umbilical vein endothelial cells induced by lipopolysaccharide and investigate its impossible mechanism. Methods Human umbilical vein endothelial cells were used to make the inflammatory injured cell model, in-vitro cultured cell were divided into normal control group, LPS model group, DMSO control group, CAPZ group, low-and high-dose evodiamine group. The cell survival rate was detected by cell counting kit-8.The contents of nitric oxide(NO) in the medium serum were detected by Elisa. The expression level of TLR4 and NF-κB p65 in various groups were detected by Western blotting method. Results Compared with control group, the cell survival rate and the contents of NO were obviously decreased, expression levels of Toll-like receptor 4(TLR4) and nuclear factor-kappa B(NF-κB) p65 was increased in LPS model group. Compared with LPS model group, the pre-treatment of Evodiamine obviously increased the cell survival rate, promoted the secretion of NO and inhibited the expressions of TLR4 and NF-κB p65. After adding transient receptor potential vanilloid 1(TRPV1) blocker, the cell survival rate was obviously decreased and expression levels of NF-κB p65 was increased compared with high-dose evodiamine group, which weakened the effects of evodamine. Conclusion Evodiamine can relieve the inflammatory injury of HUVECs induced by LPS through TRPV1, it may inhibit the TLR4/NF-κB signaling pathway and promote the cell survival rate and synthesis of NO.

关 键 词：吴茱萸碱 内皮细胞损伤 TRPV1受体 核转录因子-ΚB 

分 类 号：R285.5[医药卫生—中药学]