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Gallic acid attenuates type I diabetic nephropathy in rats
Chemico-Biological Interactions ( IF 5.1 ) Pub Date : 2018-01-10
Mayuresh Sudamrao Garud, Yogesh Anant Kulkarni

Literatures suggest that TGF-β1 have a central role in the progression of diabetic nephropathy and its down regulation can improve the disease condition. Oxidative stress, generation of advanced glycation end products and activation of renin angiotensin system are the connecting links between hyperglycemia and TGF-β1 over expression. Gallic acid is a phytochemical having wide range of biological activities. Gallic acid is reported to have antioxidant and advanced glycation inhibitory activity. It has also shown inhibitory effects on angiotensin converting enzyme. Gallic acid qualifies as a drug candidate to be tested in the diabetic nephropathy, one of the important complication of diabetes.

Streptozotocin (55 mg/kg body weight, i.p.) induced diabetic nephropathy was used as an experimental model. Gallic acid was evaluated for its possible effect at the dose of 20 and 40 mg/kg body weight.

Gallic acid treatment significantly lowered plasma levels of the creatinine and blood urea nitrogen and elevated the levels of the protein and albumin. Gallic acid also improved creatinine clearance. Determination of oxidative stress parameters showed that the oxidative stress in kidney tissues was reduced significantly in gallic acid treated animals. Results of the Plasma, urine and oxidative stress parameters were also reflected in the histo-pathological evaluation showing improvement in kidney patho-physiology. ELISA assay for circulating TGF-β1 evaluation and immunohistochemical study for determination of kidney expression of TGF-β1 revealed that gallic acid significantly lowered both the circulating and tissue levels of TGF-β1.

Results supports the hypothesis that gallic acid can be effectively used in the treatment of diabetic nephropathy.



中文翻译:

没食子酸可减轻大鼠的I型糖尿病肾病

文献表明,TGF-β1在糖尿病性肾病的进展中具有重要作用,其下调可改善疾病状况。氧化应激,高级糖基化终产物的产生以及肾素血管紧张素系统的激活是高血糖与TGF-β1过表达之间的联系。没食子酸是具有广泛生物活性的植物化学物质。没食子酸据报道具有抗氧化剂和先进的糖基化抑制活性。它也显示出对血管紧张素转化酶的抑制作用。没食子酸有资格作为糖尿病肾病(糖尿病的重要并发症之一)中待测药物的候选药物。

链脲佐菌素(55 mg / kg体重,腹腔注射)诱导的糖尿病肾病被用作实验模型。评估了没食子酸在20和40 mg / kg体重的剂量下可能产生的作用。

没食子酸处理可显着降低血浆中的肌酐和血液中尿素氮的含量,并提高蛋白质和白蛋白的含量。没食子酸还改善了肌酐清除率。氧化应激参数的测定表明,在没食子酸治疗的动物中,肾脏组织中的氧化应激显着降低。血浆,尿液和氧化应激参数的结果也反映在组织病理学评估中,显示肾脏病理生理有所改善。用ELISA法测定循环中的TGF-β1,用免疫组织化学法测定肾脏中TGF-β1的表达,结果表明没食子酸显着降低了TGF-β1的循环和组织水平。

结果支持这样的假说,没食子酸可以有效地用于糖尿病性肾病的治疗。

更新日期:2018-01-11
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