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外文期刊>Journal of King Saud University
>Oxidative stress and hepatocellular mitochondrial dysfunction attenuated by asiatic acid in streptozotocin-induced diabetic rats
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Oxidative stress and hepatocellular mitochondrial dysfunction attenuated by asiatic acid in streptozotocin-induced diabetic rats
Oxidative stress produced by mitochondria is one of the main causes for diabetes associated complications. This study was planned to assess the efficacy of asiatic acid (AA) on oxidative stress mediated hepatocellular mitochondrial dysfunction in streptozotocin (STZ)-induced type-2 diabetic rats. Diabetic rats were generated by intraperitoneal injection of STZ administered as single dose at 40?mg/kg body weight (b. wt.). Then the rats were treated with 20?mg of AA or 600?μg of glibenclamide (Glib)/kg b. wt, once in a day for 45?days. The results of this study illustrated that diabetic rat liver mitochondrial malondialdehyde (MDA), reactive oxygen species (ROS) and protein carbonyl (PCO) levels were significantly increased at the same time antioxidant enzymes and non-enzymes status was markedly diminished when compared with the liver mitochondria of normal control rats. A marked reduction in ROS, MDA, PCO and significant amelioration in non-enzymatic and enzymatic antioxidants were observed in diabetic rats treated with AA or Glib as compared with untreated diabetic control rats. Tricarboxylic acid (TCA) cycle enzymes like isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase and electron transport chain (ETC) complexes activities were significantly diminished in diabetic rats. Besides, mitochondrial uncoupling protein-2 (UCP2) expression was significantly upregulated at the same time adenosine triphosphate (ATP) level and mitochondrial membrane potential (MMP) was markedly lowered in the mitochondria of diabetic rats. AA or Glib treatment with diabetic rats restored the TCA cycle enzymes activities, ETC complexes, UCP2, MMP and ATP level to near normal control rats as compared with untreated diabetic control rats. Hence, the results of the current study indicated that AA ameliorated mitochondrial function by attenuating oxidative stress in STZ-induced type-2 diabetic rats.
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机译：线粒体产生的氧化应激是糖尿病相关并发症的主要原因之一。本研究计划评估亚洲酸（AA）对链脲佐菌素（STZ）诱导的2型糖尿病大鼠氧化胁迫介导的肝细胞线粒体功能障碍的抗氧化胁迫的疗效。通过在40×mg / kg体重（b。重量）的单剂量以单剂量施用的STZ产生糖尿病大鼠。然后用20μl或600μg的Glibenclamide（glib）/ kg b处理大鼠。 WT，一天一次持续45个月。本研究的结果说明了糖尿病大鼠肝脏线粒体丙二醛（MDA），反应性氧物质（ROS）和蛋白质羰基（PCO）水平在相同的时间显着增加，与之相比，非酶状态明显减少。正常对照大鼠肝线粒体。与未处理的糖尿病对照大鼠相比，在用AA或GLIB处理的糖尿病大鼠中观察到ROS，MDA，PCO和非酶促抗氧化剂的显着改善的显着降低。糖尿病大鼠在糖尿病大鼠中显着降低了三羧酸脱氢酶，α-酮戊二酸脱氢酶，α-酮戊二酸脱氢酶，琥珀酸脱氢酶，甘氨酸脱氢酶，苹果酸脱氢酶和电子传输链（等）复合物活性。此外，在糖尿病大鼠线粒体中，线粒体脱象蛋白-2（UCP2）表达显着上调，同时腺苷三磷酸（ATP）水平，线粒体膜电位（MMP）明显降低。与未处理的糖尿病对照大鼠相比，使用糖尿病大鼠的AA或Glib治疗恢复了TCA循环酶活性，ETC复合物，UCP2，MMP和ATP水平，接近正常对照大鼠。因此，目前研究的结果表明AA通过在STZ诱导的2型糖尿病大鼠中衰减氧化应激来改善线粒体功能。
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