中文摘要：

目的: 一份以前的报告显示出从中国植物大黄和巨大的 knotweed 根茎提取的那 emodin 能改善 anticancer 药 HEK293 房间的导致 cisplatin 的损害。在这研究，我们调查了是否并且 emodin 怎么能在 vitro.Methods 保护肾的管状的上皮的房间免于导致 cisplatin 的 nephrotoxicity : 正常老鼠的生存能力和 apoptosis 肾的管状的上皮的房间(NRK-52E ) 被检测分别地使用 formazan 试金和流动 cytometry 分析。表明小径相关的蛋白质的劈开的 caspase-3， autophagy 制造者 LC3 I/II，和 AMPK/mTOR 的表示层次与西方的污点分析被测量。形态学和 RFP-LC3 荧光的变化在 microscopy.Results 下面被观察: Cisplatin (10-50 μ； mol/L ) ， dose-dependently 在 NRK-52E 房间导致了房间损坏和 apoptosis emodin (10 和 100 μ； mol/L ) 显著地改善的导致 cisplatin 的房间损坏， apoptosis 和 caspase-3 劈开。Emodin dose-dependently 增加了 LC3-II 层次并且导致了 RFP-LC3-containing 在 NRK-52E 房间的有小斑点的结构。而且， emodin 的保护的效果被 bafilomycin A1 (10 nmol/L ) 废除，并且由 rapamycin (100 nmol/L ) 模仿了。而且， emodin 增加了 AMPK 的 phosphorylation 并且压制了 mTOR 的 phosphorylation。AMPK 禁止者混合物 C (10 μ； mol/L ) 不仅废除导致 emodin 的 autophagy 激活，而且导致 emodin 的 anti-apoptotic effects.Conclusion : Emodin 改善老鼠的导致 cisplatin 的 apoptosis 在通过 modulating 的 vitro 的肾的管状的房间表明小径并且激活 autophagy 的 AMPK/mTOR。Emodin 可以为导致 cisplatin 的 nephrotoxicity 的预防有治疗学的潜力。

英文摘要：

Aim： A previous report shows that emodin extracted from the Chinese herbs rhubarb and giant knotweed rhizome can ameliorate the anticancer drug cisplatin-induced injury of HEK293 cells. In this study, we investigated whether and how emodin could protect renal tubular epithelial cells against cisplatin-induced nephrotoxicity in vitro. Methods： The viability and apoptosis of normal rat renal tubular epithelial cells （NRK-52E） were detected using formazan assay and flow cytometry analysis, respectively. The expression levels of cleaved caspase-3, autophagy maker LC3 1/11, and AMPK/mTOR signal- ing pathway-related proteins were measured with Western blot analysis. The changes of morphology and RFP-LC3 fluorescence were observed under microscopy. Results： Cisplatin （10-50 pmol/L） dose-dependently induced cell damage and apoptosis in NRK-52E cells, whereas emodin （10 and 100 pmol/L） significantly ameliorated cisplatin-induced cell damage, apoptosis and caspase-3 cleavage. Emodin dose-dependently increased LC3-11 levels and induced RFP-LC3-containing punctate structures in NRK-52E cells. Furthermore, the protective effects of emodin were abolished by bafilomycin A1 （10 nmol/L）, and mimicked by rapamycin （100 nmol/L）. Moreover, emodin increased the phosphorylation of AMPK and suppressed the phosphorylation of mTOR. The AMPK inhibitor compound C （10 pmol/L） not only abol- ished emodin-induced autophagy activation, but also emodin-induced anti-apoptotic effects. Conclusion： Emodin ameliorates cisplatin-induced apoptosis of rat renal tubular cells in vitro through modulating the AMPK/mTOR sig- naling pathways and activating autophagy. Emodin may have therapeutic potential for the prevention of cisplatin-induced nephro- toxicity.