文献类型：期刊文献

英文题名：Triptolide improves myocardial fibrosis in rats through inhibition of nuclear factor kappa B and NLR family pyrin domain containing 3 inflammasome pathway

作者：Shen, Jianyao[1];Ma, Hailiang[1];Wang, Chaoquan[1]

机构：[1]Shaoxing Univ, Cent Hosp, Dept Cardiol, Shaoxing 312030, Peoples R China

年份：2021

卷号：25

期号：6

起止页码：533

外文期刊名：KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY

收录：SCI-EXPANDED(收录号：WOS:000713889700001)、、Scopus(收录号：2-s2.0-85119139136)、WOS

语种：英文

外文关键词：Endomyocardial fibrosis; Heart function tests;   NF-κ B pathway; NLRP3 inflammasome; Triptolide

外文摘要：Myocardial fibrosis (MF) is the result of persistent and repeated aggravation of myocardial ischemia and hypoxia, leading to the gradual development of heart failure of chronic ischemic heart disease. Triptolide (TPL) is identified to be involved in the treatment for MF. This study aims to explore the mechanism of TPL in the treatment of MF. The MF rat model was established, subcutaneously injected with isoproterenol and treated by subcutaneous injection of TPL. The cardiac function of each group was evaluated, including LVEF, LVFS, LVES, and LVED. The expressions of ANP, BNP, inflammatory related factors (IL-1(3, IL-18, TNF-a, MCP-1, VCAM1), NLRP3 inflammasome factors (NLRP3, ASC) and fibrosis related factors (TGF-(31, COL1, and COL3) in rats were dete cted. H&E staining and Masson staining were used to observe myocardial cell inflammation and fibrosis of rats. Western blot was used to detect the p-P65 and t-P65 levels in nucleoprotein of rat myocardial tissues. LVED and LVES of MF group were significantly upregulated, LVEF and LVFS were significantly downregulated, while TPL treatment reversed these trends; TPL treatment downregulated the tissue injury and improved the pathological damage of MF rats. TPL treatment downregulated the levels of inflammatory factors and fibrosis factors, and inhibited the activation of NLRP3 inflammasome. Activation of NLRP3 inflammasome or NF-xB pathway reversed the effect of TPL on MF. Collectively, TPL inhibited the activation of NLRP3 inflammasome by inhibiting NF-xB pathway, and improved MF in MF rats.