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首页> 外文期刊>The Journal of Nutritional Biochemistry >Quercetin attenuates renal ischemia/reperfusion injury via an activation of AMP-activated protein kinase-regulated autophagy pathway
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Quercetin attenuates renal ischemia/reperfusion injury via an activation of AMP-activated protein kinase-regulated autophagy pathway

机译：槲皮素通过激活AMP激活的蛋白激酶调节的自噬途径来减轻肾脏缺血/再灌注损伤

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Renal ischemia/reperfusion (I/R) is a major cause of acute renal failure. Quercetin, a flavonoid antioxidant, presents in many kinds of food. The molecular mechanism of quercetin on renal protection during I/R is still unclear. Here, we investigated the role of AMP-activated protein kinase (AMPK)-regulated autophagy in renal protection by quercetin. To investigate whether quercetin protects renal cells from I/R-induced cell injury, an in vitro model of I/R and an in vivo I/R model were used. Cell apoptosis was determined by propidium iodide/annexin V staining. Western blotting and immunofluorescence were used to determine the autophagy. AMPK expression was inhibited with appropriate short hairpin RNA (shRNA). In cultured renal tubular cell I/R model, quercetin decreased the cell injury, up-regulated the AMPK phosphorylation, down-regulated the mammalian target of rapamycin (mTOR) phosphorylation and activated autophagy during I/R. Knockdown of AMPK by shRNA transfection decreased the quercetin-induced autophagy but did not affect the mTOR phosphorylation. In I/R mouse model, quercetin decreased the increased serum creatinine level and altered renal histological score. Quercetin also increased AMPK phosphorylation, inhibited the mTOR phosphorylation and activated autophagy in the kidneys of I/R mice. These results suggest that quercetin activates an AMPK-regulated autophagy signaling pathway, which offers a protective effect in renal I/R injury. (C) 2014 Elsevier Inc. All rights reserved.
机译：肾缺血/再灌注（I / R）是急性肾衰竭的主要原因。槲皮素是一种类黄酮抗氧化剂，它存在于多种食物中。槲皮素在I / R期间保护肾脏的分子机制尚不清楚。在这里，我们调查了槲皮素对AMP激活的蛋白激酶（AMPK）调节自噬在肾脏保护中的作用。为了研究槲皮素是否能保护肾细胞免受I / R诱导的细胞损伤，使用了I / R体外模型和体内I / R模型。细胞凋亡通过碘化丙啶/ annexin V染色确定。免疫印迹和免疫荧光用于确定自噬。 AMPK表达被适当的短发夹RNA（shRNA）抑制。在培养的肾小管细胞I / R模型中，槲皮素减少细胞损伤，上调AMPK磷酸化，下调哺乳动物靶标雷帕霉素（mTOR）的磷酸化，并在I / R期间激活自噬。 shRNA转染可抑制AMPK，降低槲皮素诱导的自噬，但不影响mTOR磷酸化。在I / R小鼠模型中，槲皮素降低了血清肌酐水平的升高并改变了肾脏组织学评分。槲皮素还增加了I / R小鼠肾脏中AMPK的磷酸化，抑制了mTOR的磷酸化并激活了自噬。这些结果表明槲皮素激活了AMPK调节的自噬信号通路，在肾脏I / R损伤中提供了保护作用。 （C）2014 Elsevier Inc.保留所有权利。

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