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CJAP ›› 2016, Vol. 32 ›› Issue (3): 221-224.doi: 10.13459/j.cnki.cjap.2016.03.008

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The mechanism of irbesartan against diabetes induced myocardial fibrosis in rat model

ZHANG Guan-jun1,2, ZHANG Wei-ping1, WANG Kai-cheng2, YU Ying1, XIE Xue-feng3, GAO Qin1   

  1. 1. Department of Physiology, Bengbu Medical Cllage, Bengbu 233030;
    2. Intensive Care Unit, Huishan People's Hospital of Wuxi, Wuxi 214187;
    3. Department of Life Sciences, Bengbu Medical College, Bengbu 233030, China
  • Received:2015-01-09 Revised:2015-10-15 Online:2016-05-28 Published:2018-06-12
  • Supported by:

Abstract: Objective:To observe the protective effect of irbesartan on myocardial fibrosis in diabetic rats, and analyze the role of extracellular signal-regulated kinase (ERK) pathway in this protection. Methods:Thirty two male SD rats were randomly divided into two groups:normal control group (CON, n=10), experimental group (n=22). Twenty diabetic rats which had modelled successfully were randomly divided into two groups:diabetic group (DM, n=10), irbesartan + DM group (Ir+DM, n=10). After 8 weeks, fasting blood glucose (FBG) level, body weight (BW), the ratio of heart weight/body weight (H/B) and left ventricular weight index (LVWI) were measured. The myocardial morphological and fibrotic changes were observed by Masson staining. Col I and col Ⅲ contents were evaluated using ELISA method, and the protein expressions of ERK1/2, p-ERK1/2 in heart tissue were tested by Western blot. Results:Compared with CON group, in diabetic rats, the levels of FBG, H/B and LVWI were increased while BW was decreased. The contents of col I and col Ⅲ were increased as well as the protein expression of p-ERK1/2 and the ratio of p-ERK1/2/ERK1/2(P<0.05,P<0.01), which had the statistic differences, while ERK1/2 protein expression was not changed. Masson staining showed myocardial collagen was increased, arranged in disorder and uneven distribution. However, in Ir+ DM group, BW was increased obviously, H/B, LVWI, the contents of col I and col Ⅲ were decreased significantly (P<0.05,P<0.01), p-ERK1/2 protein expression and the ratio of p-ERK1/2/ERK1/2 were decreased (P<0.01), which had the statistic differences. Meanwhile myocardial morphology was improved significantly. Conclusion:Diabetes can induce the happening of myocardial fibrosis, and irbesartan can induce the damage of myocardial fibrosis through inhibitting the activation of ERK.

Key words: diabetes, myocardial fibrosis, irbesartan, ERK pathway, rat

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