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BioMed Research International
Volume 2015, Article ID 867140, 10 pages
Research Article

Tanshinone IIA Attenuates Renal Fibrosis after Acute Kidney Injury in a Mouse Model through Inhibition of Fibrocytes Recruitment

1Department of Nephrology, Affiliated Nanjing Drum Tower Hospital, Medical School of Nanjing University, Nanjing 21008, China
2Department of Medicine, Rhode Island Hospital, Brown University School of Medicine, Providence, RI 02903, USA
3Department of Cardiology, Affiliated Nanjing Drum Tower Hospital, Medical School of Nanjing University, Nanjing 21008, China

Received 9 October 2015; Accepted 1 December 2015

Academic Editor: Jeremiah R. Brown

Copyright © 2015 Chunming Jiang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Acute kidney injury (AKI) is associated with an increased risk of developing advanced chronic kidney disease (CKD). Yet, effective interventions to prevent this conversion are unavailable for clinical practice. In this study, we examined the beneficial effects of Tanshinone IIA on renal fibrosis in a mouse model of folic acid induced AKI. We found that Tanshinone IIA treatment significantly attenuated the folic acid elicited kidney dysfunction on days 3, 14, and 28. This effect was concomitant with a much lessened accumulation of fibronectin and collagen in tubulointerstitium 28 days after folic acid injury, denoting an ameliorated renal fibrosis. The kidney protective and antifibrotic effect of Tanshinone IIA was likely attributable to an early inhibition of renal recruitment of fibrocytes positive for both CD45 and collagen I. Mechanistically, Tanshinone IIA treatment not only markedly diminished renal expression of chemoattractants for fibrocytes such as TGF1 and MCP-1, but also significantly reduced circulating fibrocytes at the acute phase of kidney injury. These data suggested that Tanshinone IIA might be a novel therapy for preventing progression of CKD after AKI.