Exercise Training Attenuates Upregulation of p47(phox) and p67(phox) in Hearts of Diabetic Rats.
Exercise Training Attenuates Upregulation of p47(phox) and p67(phox) in Hearts of Diabetic Rats.
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DOI：
10.1155/2016/5868913
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发表时间：
2016
影响因子：
--
通讯作者：
Patel KP
中科院分区：
文献类型：
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作者：
Sharma NM;Rabeler B;Zheng H;Raichlin E;Patel KP
运动训练（ExT）目前被用作改善糖尿病患者心功能的非药物策略。然而，其有益作用的分子机制仍然知之甚少。氧化应激在糖尿病性心肌病的发病机制中起着关键作用，产生活性氧的酶系统之一是NADH/NADPH氧化酶。本研究的目的是探讨链脲佐菌素（STZ-）诱导糖尿病对心脏组织中NADPH氧化酶的关键调控亚基p47phox和p67phox表达的影响，并确定ExT是否可以减弱这些变化。STZ治疗4周后，糖尿病大鼠左心室p47phox和p67phox的表达分别增加2.3倍和1.6倍，在糖尿病发病1周后开始的ExT治疗3周后，这种增加减弱。在心房组织中，p47phox的表达增加（74%），在糖尿病大鼠中，ExT降低了p47phox的表达。此外，ExT显著降低了糖尿病大鼠心脏中升高的胶原III水平（52%）。综上所述，ExT降低了糖尿病大鼠心脏中p47phox和p67phox的表达，这可能是糖尿病心肌病中改善心内基质从而改善心功能和防止心脏重塑的潜在机制。
Exercise training (ExT) is currently being used as a nonpharmacological strategy to improve cardiac function in diabetic patients. However, the molecular mechanism(s) underlying its beneficial effects remains poorly understood. Oxidative stress is known to play a key role in the pathogenesis of diabetic cardiomyopathy and one of the enzyme systems that produce reactive oxygen species is NADH/NADPH oxidase. The goal of this study was to investigate the effect of streptozotocin- (STZ-) induced diabetes on expression of p47phox and p67phox, key regulatory subunits of NADPH oxidase, in cardiac tissues and determine whether ExT can attenuate these changes. Four weeks after STZ treatment, expression of p47phox and p67phox increased 2.3-fold and 1.6-fold, respectively, in left ventricles of diabetic rats and these increases were attenuated with three weeks of ExT, initiated 1 week after onset of diabetes. In atrial tissues, there was increased expression of p47phox (74%), which was decreased by ExT in diabetic rats. Furthermore, increased collagen III levels in diabetic hearts (52%) were significantly reduced by ExT. Taken together, ExT attenuates the increased expression of p47phox and p67phox in the hearts of diabetic rats which could be an underlying mechanism for improving intracardiac matrix and thus cardiac function and prevent cardiac remodeling in diabetic cardiomyopathy.