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Stem Cells International
Volume 2017, Article ID 1798260, 11 pages
https://doi.org/10.1155/2017/1798260
Research Article

Therapeutic Effect and Location of GFP-Labeled Placental Mesenchymal Stem Cells on Hepatic Fibrosis in Rats

1State Key Laboratory for the Diagnosis and Treatment of Infectious Diseases, First Affiliated Hospital, College of Medicine, Zhejiang University and Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, 79 Qingchun Road, Hangzhou 310003, China
2Gansu Provincial Maternity and Child-Care Hospital, 143 Qilihe North Street, Lanzhou 730050, China
3Obstetrical Department, First Affiliated Hospital, College of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou 310003, China
4Chu Kochen Honors College, Zhejiang University, 866 Yuhangtang Road, Hangzhou 310058, China

Correspondence should be addressed to Hongcui Cao; nc.ude.ujz@oacch

Received 24 January 2017; Accepted 8 March 2017; Published 12 April 2017

Academic Editor: Vladislav Volarevic

Copyright © 2017 Jiong Yu 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.

Abstract

Background. Liver fibrosis is a chronic progressive liver disease, but no established effective treatment exists except for liver transplantation. The present study was designed to investigate the effect of human placenta mesenchymal stem cells (hPMSCs) expressing green fluorescent protein (GFP) on carbon tetrachloride- (CCl4-) induced liver fibrosis in rats. Methods. Liver fibrosis was induced by subcutaneous injection with CCl4; hPMSCs were directly transplanted into rats through the caudal vein. The therapeutic efficacy of hPMSCs on liver fibrosis was measured by liver function tests, liver elastography, histopathology, Masson’s trichrome and Sirius red staining, and immunohistochemical studies. The expression levels of fibrotic markers, transforming growth factor β1 (TGF-β1) and α-smooth muscle actin (α-SMA), were assessed using real-time polymerase chain reaction. Results. We demonstrated that liver fibrosis was significantly dampened in the hPMSC transplantation group according to the Laennec fibrosis scoring system and histological data. The Sirius red-stained collagen area and the elastography score were significantly reduced in the hPMSC-treated group. Meanwhile, hPMSC administration significantly decreased TGF-β1 and α-SMA expression and enhanced liver functions in CCl4-induced fibrotic rats. Conclusion. This study indicates that transplantation of hPMSCs could repair liver fibrosis induced by CCl4 in rats, which may serve as a valuable therapeutic approach to treat liver diseases.