2. Academic Validation
  3. Dalbergioidin Ameliorates Doxorubicin-Induced Renal Fibrosis by Suppressing the TGF- β Signal Pathway

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

  • Mediators Inflamm. 2016;2016:5147571. doi: 10.1155/2016/5147571.
Xianguo Ren 1,  Yun Bo 2,  Junting Fan 3,  Maosheng Chen 4,  Daliang Xu 5,  Yang Dong 5,  Haowei He 6,  Xianzhi Ren 7,  Rong Qu 5,  Yulian Jin 5,  Weihong Zhao 2,  Changliang Xu 8
Affiliations

Affiliations

  • 1 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.
  • 2 Department of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
  • 3 School of Pharmacy, Nanjing Medical University, Nanjing, China.
  • 4 Department of Nephrology, Zhejiang Provincial People's Hospital, Hangzhou, China.
  • 5 Department of Nephrology, Anhui Provincial Children's Hospital, Hefei, China; Nanjing University of Traditional Chinese Medicine, Nanjing, China.
  • 6 Department of Urology, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China.
  • 7 Nanjing University of Traditional Chinese Medicine, Nanjing, China.
  • 8 National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China; Nanjing University of Traditional Chinese Medicine, Nanjing, China.
PMID: 28100935 DOI: 10.1155/2016/5147571
Abstract

We investigated the effect of Dalbergioidin (DAL), a well-known natural product extracted from Uraria crinita, 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 (α-SMA), fibronectin, collagen III (Col III), E-cadherin, TGF-β, 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.

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