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L-Arginine attenuates oxidative stress condition during cardiomyopathy

机译:L-精氨酸可减轻心肌病期间的氧化应激状态

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Increased production of oxygen free radicals and decreased oxidant capacity occur in coronary artery diseases (CAD). This pro-oxidant shift in intracellular redox state may induce cell death by either direct cell membrane damage by lipid peroxidation or apoptosis through activation of transcription factors. These changes occur not only in cardiomyocytes, but also in cardiac sympathetic nerves, which are very sensitive to oxidative damage. Patients with heart failure encounter reduced peripheralsup?/supblood flow at rest, during exercise and in response to endothelium-dependentsup?/supvasodilators. Current treatments of cardiomyopathy, a degenerative condition of the myocardium frequently associated with heart failure have done little to enhance patient survival. Decreased myocardial contractility and altered regulation of peripheral circulation along with oxidative conditions are important contributors to the symptoms and prognosis of the disease process. Nitric oxide formed from?L-arginine (2-amino-5 guanidinovaleric acid) metabolism insup?/supendothelial cells contributes to regulation of blood flow undersup?/supthese conditions. L-Arginine is the precursor of nitric oxide, an endogenous messenger molecule involved in a variety of endothelium-mediated physiological effects in the vascular system. In the present study, we investigated the effect of oral administration of L-arginine (3 g/day) on the intracellular redox status of the patients of ischemic cardiomyopathy aged 45-60 yrs. The enzymatic span style="mso-bidi-font-size:9.0pt" lang="EN-GB"and non-enzymatic antioxidant parameters like superoxide dismutase, catalase, total thiols span style="mso-bidi-font-size:9.0pt" lang="EN-GB"(TSH) and ascorbic acid along with pro-oxidant parameters, such as xanthine oxidase, span style="mso-bidi-font-size:9.0pt" lang="EN-GB"as well as index of oxidative stress as protein carbonyl content and malondialdehyde (a marker of lipid peroxidation) were investigated in the plasma and RBC lysate. L-Arginine (3 g/day) administration was found to improve the levels of these parameters in the patients and regulate the blood flow, as evident by the improved blood pressure of the patients. Thus, it is inferred that L-arginine attenuates the oxidative stress conditions along with maintaining the blood pressure rate of patients suffering from cardiomyopathy. /span/span/span" xml:lang="en_US
机译:增加氧自由基的产生和降低的氧化能力发生在冠状动脉疾病(CAD)中。这个细胞内氧化还原状态下的促氧化剂转变可能通过以下任何一种诱导细胞死亡通过脂质过氧化或细胞凋亡导致的直接细胞膜损伤转录因子的激活。这些变化不仅发生在心肌细胞,还有心脏交感神经中的对氧化损伤敏感。有心脏的患者故障遇到的外围?静止时血流减少运动和对依赖内皮的?血管扩张剂的反应。心肌病的当前治疗方法经常与心力衰竭相关的心肌没有做任何改善患者生存。心肌收缩力下降和调节的改变周围循环以及氧化条件很重要导致疾病过程的症状和预后。由?L-精氨酸(2-氨基-5胍基新陈代谢在?内皮细胞中的代谢?这些细胞有助于调节血流条件。 L-精氨酸是内源性一氧化氮的前体信使分子参与多种内皮介导的生理对血管系统的影响。在本研究中,我们调查了精氨酸口服(3 g /天)对细胞内的影响年龄在45-60岁之间的缺血性心肌病患者的氧化还原状态。的酶促 style =“ mso-bidi-font-size:9.0pt” lang =“ EN-GB”>以及非酶促抗氧化剂参数,例如超氧化物歧化酶,过氧化氢酶,总硫醇 style =“ mso-bidi-font-size:9.0pt” lang =“ EN-GB”>(TSH)和抗坏血酸以及促氧化剂参数,例如如黄嘌呤氧化酶, style =“ mso-bidi-font-size:9.0pt” lang =“ EN-GB”>按以及作为蛋白质羰基的氧化应激指数含量和丙二醛(脂质过氧化的标志)进行了研究在血浆和红细胞裂解物中。发现使用L-精氨酸(3克/天)可改善患者这些参数的水平并调节血液血流的改善,这可以从患者血压的改善中看出。因此,推断L-精氨酸可减轻氧化应激条件维持患有心肌病的患者的血压水平。 “ xml:lang =” zh_CN

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