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紫檀素通过抑制TGF-信号通路改善阿霉素诱导的肾纤维化。

Dalbergioidin Ameliorates Doxorubicin-Induced Renal Fibrosis by Suppressing the TGF- Signal Pathway.

作者信息

Ren Xianguo, Bo Yun, Fan Junting, Chen Maosheng, Xu Daliang, Dong Yang, He Haowei, Ren Xianzhi, Qu Rong, Jin Yulian, Zhao Weihong, Xu Changliang

机构信息

National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China; Department of Pediatrics, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China.

Department of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.

出版信息

Mediators Inflamm. 2016;2016:5147571. doi: 10.1155/2016/5147571. Epub 2016 Dec 22.

DOI:10.1155/2016/5147571
PMID:28100935
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5214096/
Abstract

We investigated the effect of Dalbergioidin (DAL), a well-known natural product extracted from , on doxorubicin- (DXR-) induced renal fibrosis in mice. The mice were pretreated for 7 days with DAL followed by a single injection of DXR (10 mg/kg) via the tail vein. Renal function was analyzed 5 weeks after DXR treatment. DXR caused nephrotoxicity. The symptoms of nephrotic syndrome were greatly improved after DAL treatment. The indices of renal fibrosis, the phosphorylation of Smad3, and the expression of alpha-smooth muscle actin (-SMA), fibronectin, collagen III (Col III), E-cadherin, TGF-, and Smad7 in response to DXR were all similarly modified by DAL. The present findings suggest that DAL improved the markers for kidney damage investigated in this model of DXR-induced experimental nephrotoxicity.

摘要

我们研究了从[具体来源未给出]中提取的一种著名天然产物——紫檀芪（DAL）对阿霉素（DXR）诱导的小鼠肾纤维化的影响。小鼠先用DAL预处理7天，然后通过尾静脉单次注射DXR（10mg/kg）。在DXR治疗5周后分析肾功能。DXR导致肾毒性。DAL治疗后肾病综合征症状得到显著改善。DAL同样改变了响应DXR的肾纤维化指标、Smad3磷酸化以及α-平滑肌肌动蛋白（α-SMA）、纤连蛋白、胶原III（Col III）、E-钙黏蛋白、转化生长因子（TGF-）和Smad7的表达。目前的研究结果表明，DAL改善了在该DXR诱导的实验性肾毒性模型中所研究的肾损伤标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/5214096/fb075e29db3d/MI2016-5147571.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/5214096/79b2bc583dce/MI2016-5147571.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/5214096/c1cc6375fbd9/MI2016-5147571.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/5214096/345513dcf87c/MI2016-5147571.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/5214096/d00cdc845eba/MI2016-5147571.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/5214096/fb075e29db3d/MI2016-5147571.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/5214096/79b2bc583dce/MI2016-5147571.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/5214096/cc2530f65757/MI2016-5147571.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/5214096/c1cc6375fbd9/MI2016-5147571.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/5214096/345513dcf87c/MI2016-5147571.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/5214096/d00cdc845eba/MI2016-5147571.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/5214096/fb075e29db3d/MI2016-5147571.006.jpg

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