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Sprague\u2010Dawley (SD<\/jats:styled-content>) rats (n = 96) were selected, and 12 of them underwent sham surgery. The remaining 84 rats were subjected to MI<\/jats:styled-content> modelling. HE<\/jats:styled-content> and MT<\/jats:styled-content> staining were carried out to estimate infract size, histopathological changes and fibrosis degree. Macrophage infiltration and cardiomyocyte apoptosis were evaluated by immunohistochemistry and TUNEL<\/jats:styled-content> staining. Reverse transcription quantitative polymerase chain reaction (RT<\/jats:styled-content>\u2010qPCR<\/jats:styled-content>) and Western blotting were used to determine the expression levels of TLR<\/jats:styled-content>4, MyD88 and NF<\/jats:styled-content>\u2010\u03baB. Serum levels of IL<\/jats:styled-content>\u20102, IL<\/jats:styled-content>\u20106, IL<\/jats:styled-content>\u20108, TNF<\/jats:styled-content>\u2010a, procollagen I Cpropeptide (PICP<\/jats:styled-content>), and procollagen III N\u2010propeptide (PIIINP<\/jats:styled-content>) were measured using enzyme\u2010linked immunosorbent assay (ELISA<\/jats:styled-content>). The heart weight\/body weight, mean arterial pressure (MAP<\/jats:styled-content>), left ventricular end\u2010systolic pressure (LVESP<\/jats:styled-content>), +dP<\/jats:styled-content>\/dt and \u2212dP<\/jats:styled-content>\/dt increased while the ventricular function and the left ventricular end\u2010diastole pressure (LVEDP<\/jats:styled-content>) decreased in MI<\/jats:styled-content> rats. Compared with the rats undergoing sham surgery, MI<\/jats:styled-content> rats showed larger infarct size, severer fibrosis, higher expression levels of TLR<\/jats:styled-content>4, NF<\/jats:styled-content>\u2010\u03baB\u2010P65, MyD88, IL<\/jats:styled-content>\u20102, IL<\/jats:styled-content>\u20106, IL<\/jats:styled-content>\u20108, TNF<\/jats:styled-content>\u2010a, PICP<\/jats:styled-content> and PIIINP<\/jats:styled-content> as well as enhanced macrophage infiltration, cardiomyocyte apoptosis. After treatment with tanshinone IIA<\/jats:styled-content> combined with LPS<\/jats:styled-content> for 4 weeks, the rats showed better condition than those treated with only LPS<\/jats:styled-content>. These results indicate that tanshinone IIA<\/jats:styled-content> attenuates MI<\/jats:styled-content> and prevents left VR<\/jats:styled-content>. Importantly, inhibition of TLR<\/jats:styled-content>4\/MyD88\/NF<\/jats:styled-content>\u2010\u03baB signalling pathway is a key step in this process.<\/jats:p>","DOI":"10.1111\/jcmm.13557","type":"journal-article","created":{"date-parts":[[2018,3,10]],"date-time":"2018-03-10T00:12:35Z","timestamp":1520640755000},"page":"3058-3072","source":"Crossref","is-referenced-by-count":48,"title":["Retracted:<\/i> Tanshinone IIA<\/scp> prevents left ventricular remodelling via the TLR<\/scp>4\/MyD88\/NF<\/scp>\u2010\u03baB signalling pathway in rats with myocardial infarction"],"prefix":"10.1111","volume":"22","author":[{"given":"Dong\u2010Mei","family":"Wu","sequence":"first","affiliation":[{"name":"Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province School of Life Science Jiangsu Normal University Xuzhou Jiangsu Province China"},{"name":"College of Health Sciences Jiangsu Normal University Xuzhou 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