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MiR-146a Ameliorates Myocarditis and Improves the Cardiac Function in EAM Rats by Inhibiting TRAF6Chinese Full Text

ZHAO Si-jia;XU Wei-qi;LIU Na;WANG Li-jun;WU Yue;ZHOU Juan;YUAN Zu-yi;Department of Cardiovascular Medicine, First Affiliated Hospital of the Medical School, Xi’an Jiaotong University, Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education,Key Laboratory of Molecular Cardiology;

Abstract: Objective To investigate the role and the mechanism of mi R-146 a which is highly expressed in activated macrophages in experimental autoimmune myocarditis(EAM), as diffusion and activation of macrophages are significant features of EAM. Methods Detection and comparison of the cardiac function and expression level of proinflammatory mediators in EAM rats that administrated with Mi R-146 a micr ON? mi RNA agomirs(mi R-146 a agomirs) or negative control reagent, respectively. Results By the mechanism that mi R-146 a could block nuclear factor kappa-light-chainenhancer of activated B cells(NF-κB) pathway by directly targeting receptor associated factor 6(TRAF6), administration of mi R-146 a agomirs could significantly attenuate the myocarditis and improve the cardiac functions. Conclusion mi R-146 a could ameliorate myocarditis by inhibiting TRAF6/NF-κB pathway in vivo.
  • DOI:

    10.16563/j.cnki.1671-6272.2015.01.008

  • Series:

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  • Classification Code:

    R542.21

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