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中国应用生理学杂志 ›› 2016, Vol. 32 ›› Issue (3): 221-224.doi: 10.13459/j.cnki.cjap.2016.03.008

• 研究论文 • 上一篇    下一篇

厄贝沙坦对抗糖尿病大鼠心肌纤维化作用及机制

张冠军1,2, 张蔚屏1, 王开成2, 于影1, 谢雪峰3, 高琴1   

  1. 1. 蚌埠医学院生理学教研室, 安徽 蚌埠 233030;
    2. 无锡市惠山区人民医院, 江苏 无锡 214187;
    3. 蚌埠医学院2012级生物科学系, 安徽 蚌埠 233030
  • 收稿日期:2015-01-09 修回日期:2015-10-15 出版日期:2016-05-28 发布日期:2018-06-12
  • 通讯作者: 高琴,Tel:0552-3175268;E-mail:bbmcgq@126.com E-mail:bbmcgq@126.com
  • 基金资助:
    国家自然科学基金(81000074);安徽省自然科学基金(1508085MH169);蚌埠医学院博士启动基金(Bykf13A05);蚌埠医学院研究生科研创新计划项目(Byycxz1303);国家大学生创新训练计划项目(201410367009)

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:
    国家自然科学基金(81000074);安徽省自然科学基金(1508085MH169);蚌埠医学院博士启动基金(Bykf13A05);蚌埠医学院研究生科研创新计划项目(Byycxz1303);国家大学生创新训练计划项目(201410367009)

摘要: 目的:观察厄贝沙坦对抗糖尿病大鼠心肌纤维化的作用,并分析细胞外调节信号激酶(ERK)通路在其中的作用。方法:健康雄性SD大鼠32只,随机分成两组:正常对照组(CON,n=10),实验组(n=22)。实验组糖尿病造模成功20只,随机分为2组(n=10):糖尿病组(DM)、厄贝沙坦+糖尿病组(Ir+DM)。8周后测定空腹血糖(FBG)水平,计算各组大鼠体重(BW)、心体比(H/B)和左室重量指数(LVWI);Masson染色观察心肌形态及纤维化的发生;ELISA检测心肌组织胶原Ⅰ(colⅠ)、胶原Ⅲ(colⅢ)含量;Western blot检测心肌组织ERK1/2、p-ERK1/2蛋白的表达。结果:与CON组相比,DM组大鼠FBG水平、H/B、LVWI显著升高,体重显著减轻,colⅠ、colⅢ含量显著增加,心肌组织p-ERK1/2蛋白表达及p-ERK1/2/ERK1/2比值增加(P<0.05,P<0.01),ERK1/2无明显变化。Masson染色显示DM组心肌胶原纤维粗大,交织成网状,排列分布不均,沉积增多。与DM组大鼠相比,厄贝沙坦干预后大鼠体重明显增加,H/B、LVWI、心肌组织colⅠ、colⅢ含量明显降低(P<0.05,P<0.01),p-ERK1/2蛋白表达及p-ERK1/2/ERK1/2比值降低(P<0.01),且心肌形态改善明显。结论:糖尿病可诱导心肌纤维化的发生,厄贝沙坦可通过抑制ERK的活化减轻糖尿病诱导的心肌纤维化损伤。

关键词: 糖尿病, 心肌纤维化, 厄贝沙坦, ERK通路, 大鼠

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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