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首页> 外文期刊>Cellular Physiology and Biochemistry >Influence of N-Acetylcysteine on Oxidative Stress in Slow-Twitch Soleus Muscle of Heart Failure Rats
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Influence of N-Acetylcysteine on Oxidative Stress in Slow-Twitch Soleus Muscle of Heart Failure Rats

机译：N-乙酰半胱氨酸对心力衰竭大鼠慢肌团比目鱼肌氧化应激的影响

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>Background: Chronic heart failure is characterized by decreased exercise capacity with early exacerbation of fatigue and dyspnea. Intrinsic skeletal muscle abnormalities can play a role in exercise intolerance. Causal or contributing factors responsible for muscle alterations have not been completely defined. This study evaluated skeletal muscle oxidative stress and NADPH oxidase activity in rats with myocardial infarction (MI) induced heart failure. Methods and Results: Four months after MI, rats were assigned to Sham, MI-C (without treatment), and MI-NAC (treated with N-acetylcysteine) groups. Two months later, echocardiogram showed left ventricular dysfunction in MI-C; NAC attenuated diastolic dysfunction. In soleus muscle, glutathione peroxidase and superoxide dismutase activity was decreased in MI-C and unchanged by NAC. 3-nitrotyrosine was similar in MI-C and Sham, and lower in MI-NAC than MI-C. Total reactive oxygen species (ROS) production was assessed by HPLC analysis of dihydroethidium (DHE) oxidation fluorescent products. The 2-hydroxyethidium (EOH)/DHE ratio did not differ between Sham and MI-C and was higher in MI-NAC. The ethidium/DHE ratio was higher in MI-C than Sham and unchanged by NAC. NADPH oxidase activity was similar in Sham and MI-C and lower in MI-NAC. Gene expression of p47phox was lower in MI-C than Sham. NAC decreased NOX4 and p22phox expression. Conclusions: We corroborate the case that oxidative stress is increased in skeletal muscle of heart failure rats and show for the first time that oxidative stress is not related to increased NADPH oxidase activity.
机译：> 背景： 慢性心力衰竭的特征是运动能力下降，疲劳和呼吸困难的早期加重。固有骨骼肌异常可以在运动不耐症中起作用。尚未完全确定导致肌肉改变的原因或贡献因素。这项研究评估了心肌梗死（MI）诱发的心力衰竭大鼠的骨骼肌氧化应激和NADPH氧化酶活性。 方法和结果： MI后四个月，将大鼠分为假手术，MI-C（未经治疗）和MI-NAC（经 N处理-乙酰半胱氨酸）组。两个月后，超声心动图显示MI-C患者左心功能不全; NAC减轻了舒张功能障碍。在比目鱼肌中，MI-C中的谷胱甘肽过氧化物酶和超氧化物歧化酶活性降低，而NAC未改变。 3-硝基酪氨酸在MI-C和Sham中相似，在MI-NAC中低于MI-C。通过二氢乙锭（DHE）氧化荧光产物的HPLC分析评估了总活性氧（ROS）的产生。 Sham和MI-C之间的2-羟基乙啶（EOH）/ DHE比值没有差异，而MI-NAC中则更高。 MI-C中的乙锭/ DHE比Sham高，而NAC则没有改变。 NADPH氧化酶活性在Sham和MI-C中相似，而在MI-NAC中则较低。 MI-C中p47 phox 的基因表达低于Sham。 NAC降低NOX4和p22 phox 表达。 结论： 我们证实了心力衰竭大鼠骨骼肌氧化应激增加的情况，并首次证明了氧化应激与NADPH氧化酶活性的增加无关。

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