Table of Contents
ISRN Hepatology
Volume 2013 (2013), Article ID 601071, 11 pages
http://dx.doi.org/10.1155/2013/601071
Research Article

Protective Effects of Guava Pulp on Cholestatic Liver Injury

1National Hepatobiliary and Enteric Surgery Research Center, Xiangya Hospital of Central South University, 87 Xiangya Road, Changsha, Hunan 410008, China
2Surgery Department, School of Medicine, Complutense University, Madrid, Spain
3Department of Nutritional Science and Food Management, The College of Health Science, Ewha Womans University, Seoul, Republic of Korea
4Division of Gastroenterology and Liver Diseases, USC Research Center for Liver Diseases, Department of Medicine, Keck School of Medicine, USC, HMR Building, 415, 2011 Zonal Avenue, Los Angeles, CA 90033, USA

Received 5 August 2013; Accepted 5 September 2013

Academic Editors: S. DeMorrow, H. Denk, M. G. Mancino, and S. Pinlaor

Copyright © 2013 Jian Peng 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. Cholestatic liver injury is a leading cause of chronic liver diseases involved with oxidative stress changes and inflammation; thus, antioxidant and anti-inflammation compound-rich guava may play a pivotal role in protecting against the cholestatic liver damages. Our aims for this study are to determine whether guava pulp (GP) has protective effects on cholestatic liver injury-induced mouse model and on interleukin-6 (IL-6) mediated proliferation of QBC939 cholangiocarcinoma cell line. Methods. Mice were induced to cholestatic liver damage by left and median bile duct ligation (LMBDL) surgery and then treated with GP. Plasma and liver samples were collected for biochemical and pathological assays. 5-Bromo-2′-deoxyuridine (BrdU) assay and Western blots were used to detect proliferation and gene expression in QBC939 cells, respectively. Results. Compared with LMBDL only group, in GP-treated mice, the levels of alanine aminotransferase (ALT) and bilirubin decreased, biliary epithelial cell proliferation and liver fibrogenesis were suppressed, Src/MEK/ERK1/2/c-Myc pathway and expressions of transforming growth factor β1(TGF-β1), tissue inhibitor of metalloproteinases TIMP), and procollagen 1α1(COL1α1) were downregulated significantly. Moreover, the GP extract reduced IL-6-enhanced QBC939 cell proliferation, p-ERK, and c-Myc expression as well. Conclusions. GP may provide a new perspective for the treatment of cholestatic liver injury.