芒果苷对链脲佐菌素诱导的糖尿病大鼠组织中氧化应激和抗氧化状态的保护作用

ISRN Pharmacology Pub Date : 2013-09-12 eCollection Date: 2013-01-01 DOI:10.1155/2013/750109
Periyar Selvam Sellamuthu, Palanisamy Arulselvan, Subban Kamalraj, Sharida Fakurazi, Murugesan Kandasamy
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摘要

氧化应激在糖尿病并发症的发展过程中起着重要作用。本研究旨在通过测量肝脏和肾脏中的氧化指标以及改善特性,探讨口服芒果苷对链脲佐菌素(STZ)诱导的糖尿病大鼠的有益影响。糖尿病大鼠服用芒果苷后,血糖明显降低,血浆胰岛素水平明显升高。与正常对照组相比,糖尿病对照组大鼠肝脏和肾脏组织中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)等抗氧化酶的活性以及还原型谷胱甘肽(GSH)的水平明显降低(P < 0.05),而脂质过氧化(LPO)指标的水平则有所增加。连续 30 天口服芒果苷(40 毫克/千克体重/天)对研究的所有生化指标和氧化指标都有显著的改善作用。接受芒果苷治疗的糖尿病大鼠的肝脏和肾脏组织结构几乎恢复正常,组织病理学检查证实了这一点。这些结果表明,芒果苷除了对实验诱导的糖尿病大鼠具有抗糖尿病作用外,还具有潜在的改善作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Protective nature of mangiferin on oxidative stress and antioxidant status in tissues of streptozotocin-induced diabetic rats.

Oxidative stress plays an important role in the progression of diabetes complications. The aim of the present study was to investigate the beneficial effect of oral administration of mangiferin in streptozotocin (STZ)-induced diabetic rats by measuring the oxidative indicators in liver and kidney as well as the ameliorative properties. Administration of mangiferin to diabetic rats significantly decreased blood glucose and increased plasma insulin levels. The activities of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) and level of reduced glutathione (GSH) were significantly (P < 0.05) decreased while increases in the levels of lipidperoxidation (LPO) markers were observed in liver and kidney tissues of diabetic control rats as compared to normal control rats. Oral treatment with mangiferin (40 mg/kg b.wt/day) for a period of 30 days showed significant ameliorative effects on all the biochemical and oxidative parameters studied. Diabetic rats treated with mangiferin restored almost normal architecture of liver and kidney tissues, which was confirmed by histopathological examination. These results indicated that mangiferin has potential ameliorative effects in addition to its antidiabetic effect in experimentally induced diabetic rats.

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