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CJAP ›› 2018, Vol. 34 ›› Issue (1): 16-18.doi: 10.12047/j.cjap.5572.2018.005

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Effects of total flavonids of astragalus on arrhythmia,endoplasmic reticulum stress in mice with viral myocarditis

LIU Hao1, HURILE Bate1, XIONG Ying2, WEI Cheng-xi3, XUAN Li-ying3, WANG Yu3, ZHAO Ming1   

  1. 1. Affiliated Hospital of Inner Mongolia University for Nationalities, Tongliao 028000;
    2. the First Clinical College of Inner Mongolia Medical University, Hohhot 100059;
    3. Medical College of Inner Mongolia University for Nationalities, Tongliao 028000, China
  • Received:2017-02-27 Revised:2017-10-24 Online:2018-01-28 Published:2018-06-19
  • Supported by:

Abstract: Objective: To investigate the effects of total flavonids of astragalus(TFA) on arrhythmia, endoplasmic reticulum stress and connexcin in mice with viral myocarditis and to clarify the mechanisms of TFA against viral myocarditis complicated with arrhythmia.Methods: Thirty-six male Balb/c mice were randomly divided into control group, viral myocarditis group and total flavonoids group (n=12). The mice of viral myocarditis were intraperitonealy injected with 0.1 ml/day 10-950 TCID CVB3 for 3 days. The mice of TFA group were intraperitoneal injected with 0.1 ml/day 10-950 TCID CVB3 for 3 days and treated with 0.1ml, 20 mg/L TFA by tail vein injection. At the end of the experiment, arrhythmia was detected by electrocardiogram, the heart of mice were stained by HE, the expressions of glucose-regulated protein 78(GRP78), endoplasmic reticulum stress signaling pathway factor activating transcription factor 4(ATF4) and connexcin 43(Cx43) were detected by Western blot.Results: The expressions of GRP78 and ATF4 were increased and the expression of Cx43 was decreased in viral myocarditis, while TFA inhibited these effect of viral myocarditis in heart of mice.Conclusion: The antiarrhythmic effect of TFA may be related to the alleviation of endoplasmic reticulum stress and the increase of Cx43 expression.

Key words: viral myoearditis, arrhythmia, endoplasmic reticulum stress, gap junction protein, mice

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