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首页> 外文期刊>Journal of Cellular Physiology >Curcumin alleviates ischemia reperfusion-induced late kidney fibrosis through the APPL1/Akt signaling pathway
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Curcumin alleviates ischemia reperfusion-induced late kidney fibrosis through the APPL1/Akt signaling pathway

机译:姜黄素减轻缺血reperfusion-induced通过APPL1 / Akt晚期肾脏纤维化信号通路

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摘要

As a major cause of renal failure, transient renal ischemia and reperfusion induce both acute kidney injury and late fibrosis, which are the common pathological manifestations of end-stage renal disease. Curcumin is a biologically active polyphenolic compound found in turmeric. Increasing evidence has demonstrated that curcumin has a protective action against renal fibrosis, whereas mechanisms underlying the anti-fibrosis role of curcumin remain poorly defined. Here, we found that APPL1, an important intracellular binding partner for AdipoR, was involved in the pathogenesis of acute injury or fibrosis and was significantly upregulated by curcumin in a mouse model of ischemia reperfusion-induced late kidney fibrosis. Moreover, Akt signaling was the specific signaling pathway identified downstream of APPL1 in the pathogenesis of fibrosis. Our in vitro experiment demonstrated that curcumin alleviates ischemia reperfusion-induced late kidney fibrosis via the APPL1/Akt pathway. These data are helpful for understanding the anti-fibrosis mechanism of curcumin in the pathogenesis of AKI-induced late fibrosis.
机译:肾功能衰竭的主要原因,短暂的肾急性肾脏缺血和再灌注诱导损伤和纤维化,是常见的终末期肾的病理表现疾病。姜黄中含有的多酚化合物。越来越多的证据证明姜黄素对肾脏具有保护行动纤维化,而机制姜黄素的抗纤维化作用仍然不佳定义的。细胞内具有约束力的合作伙伴AdipoR,参与急性损伤的发病机制纤维化和显著调节姜黄素在小鼠模型的缺血reperfusion-induced晚期肾脏纤维化。此外,一种蛋白激酶信号是特定的信号通路下游APPL1识别在肝纤维化的发病机制。实验表明,姜黄素能缓解缺血reperfusion-induced晚期肾脏纤维化通过APPL1 / Akt通路。对于理解的抗纤维化机制姜黄素的病机AKI-induced迟了纤维化

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