作者: Chengchuang Zhan , Nan Bai , Min Zheng , Yanyan Wang , Yuanqi Wang
DOI: 10.1016/J.LFS.2020.118984
关键词: Oxidative stress 、 Angiotensin II 、 Doxorubicin 、 Chymase 、 Heart disease 、 Pharmacology 、 Fibrosis 、 Apoptosis 、 Chemistry 、 Tranilast
摘要: An increase in oxidative stress is an important pathological mechanism of heart injury induced by doxorubicin (DOX). Tranilast anti-allergy drug that has been shown to possess good antioxidant activity previous studies. The overexpression and secretion chymase mast cells (MCs) the angiotensin II (Ang II), which plays a crucial role myocardial hypertrophy deterioration disease. MC stabilizer tranilast (N-(3,4-dimethoxycinnamoyl) anthranilic acid; tran) prevents from degranulating, may reduce DOX-induced Ang synthesis. Therefore, present study, we hypothesized will protect rats damage via its activity, thereby inhibiting expression. Thirty male Wistar were divided into three groups (n = 10 each group) received DOX, combination DOX or saline (the control test this hypothesis. suppressed expression, reduced levels prevented function DOX. Based on findings suppression chymase-dependent Ang-II production direct effect inhibition apoptosis fibrosis because capacity contribute protective against hypertrophy.