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Tranilast prevents doxorubicin-induced myocardial hypertrophy and angiotensin II synthesis in rats.

Life sciences (2021-01-01)
Chengchuang Zhan, Nan Bai, Min Zheng, Yanyan Wang, Yuanqi Wang, Li Zhang, Jianqiang Li, Guangnan Li, Hongyan Zhao, Guangzhong Liu, Qi Lou, Wen Yang, Tiankai Li, Luyifei Li, Weimin Li
ABSTRACT

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

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Tranilast, ≥98% (HPLC), powder
Sigma-Aldrich
(+)-Biotin 4-nitrophenyl ester, 98%
Sigma-Aldrich
Anti-ST2 antibody produced in rabbit, affinity isolated antibody, buffered aqueous solution