Celastrol ameliorates cisplatin nephrotoxicity by inhibiting NF-κB and improving mitochondrial function.
Celastrol ameliorates cisplatin nephrotoxicity by inhibiting NF-κB and improving mitochondrial function.
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Celastrol 通过抑制 NF-kappaB 和改善线粒体功能来改善顺铂肾毒性。
DOI：
10.1016/j.ebiom.2018.09.031
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发表时间：
2018-10
期刊：
影响因子：
11.1
通讯作者：
Jia Z
中科院分区：
文献类型：
--
作者：
Yu X;Meng X;Xu M;Zhang X;Zhang Y;Ding G;Huang S;Zhang A;Jia Z
Celastrol is an active ingredient of Chinese medicine Tripterygium wilfordii which is clinically used to treat the immune diseases. Currently, celastrol is documented as a potent agent for treating cancer and inflammatory disorders. This study was to investigate the effect of celastrol on cisplatin nephrotoxicity and the underlying mechanism. Male C57BL/6 mice were treated with cisplatin (20 mg/kg) with or without celastrol treatment (1 and 2 mg/kg/day). In vitro, human proximal tubule epithelial cell line (HK−2) and mouse renal tubule epithelial cells (RTECs) were treated with cisplatin (5 μg/mL) with or without celastrol administration. Then renal injury and cell damage were evaluated. In vivo, after celastrol treatment, cisplatin-induced kidney injury was significantly ameliorated as shown by the improvement of renal function (BUN, serum creatinine, and cystatin C), kidney morphology (PAS staining) and oxidative stress (MDA) and the suppression of renal tubular injury markers of KIM-1 and NGAL. Meanwhile, the renal apoptosis and inflammation induced by cisplatin were also strikingly attenuated in celastrol-treated mice. In vitro, celastrol treatment markedly inhibited cisplatin-induced renal tubular cell apoptosis, suppressed NF-κB activation, and improved mitochondrial function evidenced by the restored mtDNA copy number, mitochondrial membrane potential, and OXPHOS activity in cisplatin-treated renal tubular epithelial cells. This work suggested that celastrol could protect against cisplatin-induced acute kidney injury possibly through suppressing NF-κB and improving mitochondrial function. The National Natural Science Foundation of China, National Key Research and Development Program, and Natural Science Foundation of Jiangsu Province.
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影响因子：
5.2
作者：
Hoek J;Bloemendal KM;van der Velden LA;van Diessen JN;van Werkhoven E;Klop WM;Tesselaar ME
通讯作者：
Tesselaar ME
影响因子：
29
作者：
Baker RG;Hayden MS;Ghosh S
通讯作者：
Ghosh S
雷公藤红素诱导的 Nur77 与 TRAF2 相互作用通过促进线粒体泛素化和自噬减轻炎症
影响因子：
16
作者：
Hu M;Luo Q;Alitongbieke G;Chong S;Xu C;Xie L;Chen X;Zhang D;Zhou Y;Wang Z;Ye X;Cai L;Zhang F;Chen H;Jiang F;Fang H;Yang S;Liu J;Diaz-Meco MT;Su Y;Zhou H;Moscat J;Lin X;Zhang XK
通讯作者：
Zhang XK
影响因子：
7.5
作者：
Abu Bakar, Mohamad Hafizi;Tan, Joo Shun
通讯作者：
Tan, Joo Shun
影响因子：
4.5
作者：
Domitrovic, Robert;Cvijanovic, Olga;Skoda, Marko
通讯作者：
Skoda, Marko