Open AccessRetracted: Tanshinone IIA prevents left ventricular remodelling via the TLR 4/MyD88/ NF ‐κB signalling pathway in rats with myocardial infarction
Author(s) -
Wu DongMei,
Wang YongJian,
Han XinRui,
Wen Xin,
Li Lei,
Xu Lan,
Lu Jun,
Zheng YuanLin
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13557
Subject(s) - tunel assay , myocardial fibrosis , fibrosis , ventricular remodeling , myocardial infarction , apoptosis , ventricular pressure , chemistry , medicine , immunohistochemistry , real time polymerase chain reaction , nf κb , endocrinology , blood pressure , biochemistry , gene
Abstract In this study, we aim to investigate the role of tanshinone IIA in myocardial infarction ( MI ), especially in left ventricular remodelling ( VR ) and the underlying mechanism involving the TLR 4/MyD88/ NF ‐κB signalling pathway. Sprague‐Dawley ( SD ) rats (n = 96) were selected, and 12 of them underwent sham surgery. The remaining 84 rats were subjected to MI modelling. HE and MT staining were carried out to estimate infract size, histopathological changes and fibrosis degree. Macrophage infiltration and cardiomyocyte apoptosis were evaluated by immunohistochemistry and TUNEL staining. Reverse transcription quantitative polymerase chain reaction ( RT ‐ qPCR ) and Western blotting were used to determine the expression levels of TLR 4, MyD88 and NF ‐κB. Serum levels of IL ‐2, IL ‐6, IL ‐8, TNF ‐a, procollagen I Cpropeptide ( PICP ), and procollagen III N‐propeptide (PIII NP ) were measured using enzyme‐linked immunosorbent assay ( ELISA ). The heart weight/body weight, mean arterial pressure ( MAP ), left ventricular end‐systolic pressure ( LVESP ), + dP /dt and − dP /dt increased while the ventricular function and the left ventricular end‐diastole pressure ( LVEDP ) decreased in MI rats. Compared with the rats undergoing sham surgery, MI rats showed larger infarct size, severer fibrosis, higher expression levels of TLR 4, NF ‐κB‐P65, MyD88, IL ‐2, IL ‐6, IL ‐8, TNF ‐a, PICP and PIII NP as well as enhanced macrophage infiltration, cardiomyocyte apoptosis. After treatment with tanshinone IIA combined with LPS for 4 weeks, the rats showed better condition than those treated with only LPS . These results indicate that tanshinone IIA attenuates MI and prevents left VR . Importantly, inhibition of TLR 4/MyD88/ NF ‐κB signalling pathway is a key step in this process.