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首页> 外文期刊>The Journal of Nutritional Biochemistry >Antioxidant treatment protects diabetic rats from cardiac dysfunction by preserving contractile protein targets of oxidative stress.
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Antioxidant treatment protects diabetic rats from cardiac dysfunction by preserving contractile protein targets of oxidative stress.

机译：抗氧化剂治疗可通过保留氧化应激的收缩蛋白靶标来保护糖尿病大鼠免于心脏功能障碍。

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Backgound. Animal studies suggest that reactive oxygen species (ROS) play an important role in the development of diabetic cardiomyopathy. Hypothesis. Matrix metalloproteinase-2 (MMP-2) is activated by ROS and contributes to the acute loss of myocardial contractile function by targeting and cleaving susceptible proteins including troponin I (TnI) and alpha-actinin. Methods. Using the streptozotocin-induced diabetic rat model, we evaluated the effect of daily in vivo administration of sodium selenate (0.3 mg/kg; DMS group), or a pure omega-3 fish oil with antioxidant vitamin E (omega-3E; 50 mg/kg; DMFA group), which has antioxidant-like effects, for 4 weeks on heart function and on several biochemical parameters related to oxidant stress and MMP-2. Results. Although both treatments prevented the diabetes-induced depression in left ventricular developed pressure (LVDP) as well as the rates of changes in developed pressure (+or-dP/dt) (P<.001), the improvement in LVDP of the DMS group was greater compared to that of the DMFA group (P<.001). Moreover, these treatments reduced the diabetes-induced increase in myocardial oxidized protein sulfhydryl and nitrite concentrations (P<.001). Gelatin zymography and Western blot data indicated that the diabetes-induced changes in myocardial levels of MMP-2 and tissue inhibitor of matrix metalloproteinase-4 (TIMP-4) and the reduction in TnI and alpha-actinin protein levels were improved in both the DMS and DMFA groups (P<.001). Conclusions. These results suggest that diabetes-induced alterations in MMP-2 and TIMP-4 contribute to myocardial contractile dysfunction by targeting TnI and alpha-actinin and that sodium selenate or omega-3E could have therapeutic benefits in diabetic cardiomyopathy.
机译：背景。动物研究表明，活性氧（ROS）在糖尿病性心肌病的发展中起重要作用。假设。基质金属蛋白酶2（MMP-2）被ROS激活，并通过靶向和裂解包括肌钙蛋白I（TnI）和α-肌动蛋白在内的易感蛋白而导致心肌收缩功能的急性丧失。方法。使用链脲佐菌素诱导的糖尿病大鼠模型，我们评估了每天体内给予硒酸钠（0.3 mg / kg; DMS组）或具有抗氧化剂维生素E的纯omega-3鱼油（omega-3E; 50 mg）的效果/ kg; DMFA组），对心脏功能以及与氧化应激和MMP-2有关的几个生化参数具有类似抗氧化剂的作用，持续4周。结果。尽管两种治疗均能预防糖尿病引起的左心室发育压力（LVDP）降低以及发展压力变化率（+或-dP / dt）（P <.001），但DMS组的LVDP有所改善与DMFA组相比更大（P <.001）。此外，这些治疗减少了糖尿病引起的心肌氧化蛋白巯基和亚硝酸盐浓度的增加（P <.001）。明胶酶谱和Western印迹数据表明，DMS均改善了糖尿病引起的心肌MMP-2和基质金属蛋白酶4（TIMP-4）组织抑制剂的心肌水平变化以及TnI和α-肌动蛋白水平的降低和DMFA组（P <.001）。结论。这些结果表明，糖尿病引起的MMP-2和TIMP-4改变通过靶向TnI和α-肌动蛋白而导致心肌收缩功能障碍，硒酸钠或omega-3E在糖尿病性心肌病中具有治疗作用。

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