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二羟丙酮基肌醇减轻链脲佐菌素诱导的糖尿病大鼠氧化应激及肝组织超微结构改变。

Attenuation of oxidative stress and alteration of hepatic tissue ultrastructure by D-pinitol in streptozotocin-induced diabetic rats.

机构信息

Department of Biochemistry, University of Madras, Guindy Campus, Chennai 600 025, Tamilnadu, India.

出版信息

Free Radic Res. 2010 Jun;44(6):668-78. doi: 10.3109/10715761003733901.

DOI:10.3109/10715761003733901
PMID:20370563
Abstract

The present study was aimed to investigate the effect of D-pinitol on hyperglycaemia mediated oxidative stress by analysing the hepatic antioxidant competence, pro-inflammatory cytokines and ultrastructural changes in liver tissues of streptozotocin-induced diabetic rats. Oral administration of D-pinitol (50 mg/kg b.w.) resulted in significant (p < 0.05) attenuation in blood glucose, glycosylated haemoglobin and pro-inflammatory markers such as TNF-alpha, IL-1beta, IL-6, NF-kappaB p65 unit and NO and significant (p < 0.05) elevation in the plasma insulin level. In addition, D-pinitol instigated a significant escalation in the levels of hepatic tissue non-enzymatic antioxidants and the activities enzymatic antioxidants of diabetic rats with significant (p < 0.05) decrease in lipid peroxides and hydroperoxides formation, thus demonstrating the protective role of D-pinitol on the hepatic tissues from oxidative stress-induced liver damage. These biochemical observations were complemented by histological and ultrastructural examination of liver section. Thus, the present study demonstrates the hepatoprotective nature of D-pinitol by attenuating hyperglycaemia-mediated pro-inflammatory cytokines and oxidative stress.

摘要

本研究旨在通过分析链脲佐菌素诱导的糖尿病大鼠肝脏组织的抗氧化能力、促炎细胞因子和超微结构变化,研究 D-松醇对高血糖介导的氧化应激的影响。D-松醇(50mg/kg b.w.)经口给药可显著降低(p<0.05)血糖、糖化血红蛋白和促炎标志物如 TNF-α、IL-1β、IL-6、NF-κB p65 亚单位和 NO,并显著升高(p<0.05)血浆胰岛素水平。此外,D-松醇可显著提高糖尿病大鼠肝组织中非酶抗氧化剂水平和酶抗氧化剂活性,降低脂质过氧化物和氢过氧化物的形成,从而证明 D-松醇对肝组织氧化应激损伤具有保护作用。这些生化观察结果得到了肝组织切片的组织学和超微结构检查的补充。因此,本研究表明 D-松醇通过减轻高血糖介导的促炎细胞因子和氧化应激具有肝保护作用。

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