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游泳运动通过TGF-β1/Smad3通路改善自发性高血压大鼠心肌间质纤维化研究*
引用本文:曹〓姣.游泳运动通过TGF-β1/Smad3通路改善自发性高血压大鼠心肌间质纤维化研究*[J].广州体育学院学报,2018(5):106-112.
作者姓名:曹〓姣
作者单位:(广东第二师范学院 体育学院,广东 广州〓510303)
基金项目:广东省体育局科研项目(GDSS2016115);广东第二师范学院博士科研专项经费研究项目(2015ARF14);广东第二师范学院校级质量工程项目(2016ybzz05)。
摘    要:目的:观察游泳运动对自发性高血压大鼠心肌间质形态学及TGF-β1/Smad3信号通路的影响。方法:选取8只SPF级雄性WKY大鼠为正常对照组(C组);20只SPF级自发性高血压大鼠随机分为模型组(H组)和SHR+运动组(EH组),每组均10只,各组大鼠给予普通饲料喂养。运动组大鼠进行为期12周不负重游泳训练,每周训练6天,休息1天。第1周为适应性训练,从第2周开始维持60 min/d的运动时间至12周结束。干预周期结束后检测检测各组大鼠CVF%、col I和col III;QRT-PCR检测心肌Smad3,放免法检测AngII,Western-blot法检测NOX2、TGF-β1、HSP90蛋白表达。结果:(1)C组比较,H组大鼠心肌CVF%、colI、colIII、血浆AngII、心肌AngII、心肌NOX2、TGF-β1、Smad3mRNA、HSP90表达显著性增加(P<0.05或P<0.01);与H组比较,EH组大鼠除了心肌HSP90蛋白表达显著性增加外(P<0.05),其余指标均显著性降低(P<0.05或P<0.01)。结论:游泳运动能较好降低SHR大鼠心肌col I和col III蛋白表达水平,改善心肌间质纤维化,主要通过降低AngII介导NOX2表达,抑制下游TGF-β1/Smad3通路激活,其中HSP90作为其上游因子,在其中可能起着重要的调节作用。

关 键 词:游泳运动  高血压  心肌间质纤维化  TGF-β1/Smad3  HSP90
修稿时间:2018/5/11 0:00:00

Improving Myocardial Interstitial Fibrosis of Spontaneously Hypertensive Rats through TGF-beta1 / Smad3 Pathway by Swimming
CAO Jiao.Improving Myocardial Interstitial Fibrosis of Spontaneously Hypertensive Rats through TGF-beta1 / Smad3 Pathway by Swimming[J].Journal of Guangzhou Physical Education Institute,2018(5):106-112.
Authors:CAO Jiao
Institution:( Department of Physical Education, Guangdong University of Education,Guangzhou 510303,China)
Abstract:Objective: To observe the effects of swimming on TGF -beta1/Smad3 signaling in the ameriation process of myocardial interstitial remodeling of spontaneously hypertensive rats.Methods: SPF male WKY rats were chosen as group C(n=8), and SPF spontaneously hypertensive rats were divided into group model control (group H), group SHR + exercise (group EH). The number of each group was 10. Rats in each group were fed on ordinary food. Exercise group rats were arranged to no-load swimming training for 12 weeks, and 6 days a week. Fitness training for 1 week before formal training. Rats arraged to swim 60min per day from week 2 to 12 weeks. CVF%, colI and colIII were tested by Immunohistochemistry, myocardial Smad3 by QRT-PCR, and NOX2, TGF-beta 1, HSP90 protein expression by western-blot. Results: (1)Compared with group C, myocardial CVF %, colI, colIII protein expression, blood plasma AngII, myocardial AngII, myocardial NOX2 protein expression, TGF-beta 1 protein expression , Smad3mRNA level and HSP90 protein expression in rats group SHR significantly increased (P<0.05 or P<0.01); (2) Compared with group SHR, 12-week swimming could significantly reduce myocardial CVF%, colI, colIII protein expression ,plasma AngII, myocardial AngII ,NOX2 protein expression, TGF-beta 1 protein expression and Smad3 mRNA (P < 0.05),increase HSP90 protein expression (P < 0.05).Conclusions:Swimming could reduce colI and colIII protein expression in hearts of SHR, ameliorate myocardial interstitial fibrosis, mainly by reducing AngII mediated NOX2 protein expression, and inhibiting downstream TGF- beta1/Smad3 pathways, in which HSP90 as its upstream factor may play an important role .
Keywords:swimming  spontaneously hypertensive rats  interstitial fibrosis  TGF-beta1/smad3  HSP90
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