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首页> 外文期刊>RSC Advances >Quercetin ameliorates podocyte injury via inhibition of oxidative stress and the TGF-β1/Smad pathway in DN rats
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Quercetin ameliorates podocyte injury via inhibition of oxidative stress and the TGF-β1/Smad pathway in DN rats

机译：槲皮素通过抑制氧化应激和DN大鼠的TGF-β1/ Smad途径改善足细胞损伤

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An increasing number of investigations have revealed that podocytes play a crucial role in the development and progression of diabetic nephropathy (DN). Quercetin (2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-4 H -chromen-4-one) is the most common flavonol in the diet and is one of the most prominent dietary antioxidants, which might have a protective effect on DN. The present study was designed to investigate the protective effect of quercetin on podocyte impairment in a rat model of DN, as well as underlying molecular mechanisms. All diabetic rats were induced by a single intraperitoneal injection of streptozotocin, and quercetin was administered daily at a dose of 50 mg kg ~(?1) or 100 mg kg ~(?1) for 12 weeks. In the present study, quercetin markedly decreased blood glucose levels, kidney-to-body weight ratio, albuminuria, creatinine clearance rate, blood urea nitrogen, and triglycerides and significantly attenuated oxidative stress. Moreover, quercetin was observed to inhibit podocyte effacement and decrease the thickness of glomerular basement membranes. Mechanistically, quercetin significantly increased the expression of podocyte-specific markers nephrin and podocin and decreased expression of the podocyte injury marker desmin in DN rats. Quercetin also inhibited activation of the TGF-β1/Smad signaling pathway in DN rats by decreasing expression of TGF-β1, p-Smad2, and p-Smad3, and increasing Smad7 expression. These findings suggest that quercetin administration ameliorated podocyte injury in DN rats, possibly by inhibiting oxidative stress and the TGF-β1/Smad signaling pathway. Thus, quercetin may be manipulated to act as a potential drug for prevention of early diabetic nephropathy.
机译：越来越多的研究表明，足细胞在糖尿病性肾病（DN）的发展和进程中起着至关重要的作用。槲皮素（2-（3,4-二羟基苯基）-3,5,7-三羟基-4 H-铬-4--4-酮）是饮食中最常见的黄酮醇，也是最重要的饮食抗氧化剂之一，可能含有对DN的保护作用。本研究旨在研究槲皮素对DN大鼠模型中足细胞损伤的保护作用以及潜在的分子机制。腹膜内注射链脲佐菌素诱导所有糖尿病大鼠，并以50 mg kg〜（？1）或100 mg kg〜（？1）的剂量每天服用槲皮素，持续12周。在本研究中，槲皮素显着降低了血糖水平，肾脏与体重比，白蛋白尿，肌酐清除率，血液尿素氮和甘油三酸酯，并显着减轻了氧化应激。此外，观察到槲皮素可抑制足细胞剥脱并减少肾小球基底膜的厚度。从机理上讲，槲皮素显着增加了DN大鼠足细胞特异性标志物nephrin和podocin的表达，并降低了足细胞损伤标志物desmin的表达。槲皮素还通过降低TGF-β1，p-Smad2和p-Smad3的表达并增加Smad7的表达来抑制DN大鼠中TGF-β1/ Smad信号通路的激活。这些发现表明，槲皮素给药可通过抑制氧化应激和TGF-β1/ Smad信号传导途径减轻DN大鼠的足细胞损伤。因此，槲皮素可以被操纵为预防早期糖尿病肾病的潜在药物。

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