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Tanshinone IIA protects against subclinical lipopolysaccharide induced cardiac fibrosis in mice through inhibition of NADPH oxidase.

Abstract：

:Myocardial fibrosis plays a central role in the development of heart failure. It has been shown that recurrent exposure to subclinical lipopolysaccharide (LPS) increases mortality and induces cardiac fibrosis in mice, which is not mediated by the common renin-angiotensin system. LPS increased NADPH oxidase2 (NOX2) in isolated adult mouse cardiac fibroblasts and NOX2 may mediate LPS-induced cardiac fibrosis. Therefore, the current study was designed to delineate the role of NOX2 in LPS-induced fibrosis model and to investigate the preventive role of Tanshinone IIA (TIIA) on the development of cardiac fibrosis. The protective mechanism of TIIA was determined to be associated with the inhibition of NOX2, by comparing its effects with the NADPH oxidase inhibitor, apocynin. The results revealed remarkable effects of apocynin and TIIA on attenuating the development of myocardial fibrosis and fibrosis-related genes and mediators. Furthermore, TIIA and apocynin decreased the expression of NADPH oxidase subunits (NOX2 and P67phox) expression and the ROS levels. The anti-fibrotic effect of apocynin suggested that NOX2 inhibition may be a potential preventive strategy for attenuating the progression of LPS-induced cardiac fibrosis. Our results demonstrate that TIIA may be a potent agent against subclinical LPS-induced cardiac fibrosis in mice partially via inhibition of NADPH oxidase 2.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Huang L,Zhu J,Zheng M,Zou R,Zhou Y,Zhu M

doi

10.1016/j.intimp.2018.04.036

subject

Has Abstract

pub_date

2018-07-01 00:00:00

pages

59-63

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(18)30187-5

journal_volume

60

pub_type

杂志文章

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