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Oxidative Medicine and Cellular Longevity
Volume 2014 (2014), Article ID 674690, 10 pages
Research Article

BL153 Partially Prevents High-Fat Diet Induced Liver Damage Probably via Inhibition of Lipid Accumulation, Inflammation, and Oxidative Stress

1College of Bioengineering, Chongqing University, Chongqing 400044, China
2The Chinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences & Key Laboratory of Biotechnology Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, China
3Department of Pediatrics of the University of Louisville, The Kosair Children’s Hospital Research Institute, Louisville, KY 20202, USA
4Rui’an Center of the Chinese-American Research Institute for Diabetic Complications, The Third Affiliated Hospital of the Wenzhou Medical University, Wenzhou 325200, China
5Department of Cardiology at the First Hospital & School of Public Health, Jilin University, Changchun 130021, China
6Bioland Biotec Co., Ltd., Zhangjiang Modern Medical Device Park, Pudong, Shanghai 201201, China
7Bioland R&D Center, 59 Songjeongni 2-gil, Byeongcheon, Dongnam, Cheonan, Chungnam 330-863, Republic of Korea

Received 9 December 2013; Accepted 20 February 2014; Published 3 April 2014

Academic Editor: Si Jin

Copyright © 2014 Jian Wang 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.


The present study was to investigate whether a magnolia extract, named BL153, can prevent obesity-induced liver damage and identify the possible protective mechanism. To this end, obese mice were induced by feeding with high fat diet (HFD, 60% kcal as fat) and the age-matched control mice were fed with control diet (10% kcal as fat) for 6 months. Simultaneously these mice were treated with or without BL153 daily at 3 dose levels (2.5, 5, and 10 mg/kg) by gavage. HFD feeding significantly increased the body weight and the liver weight. Administration of BL153 significantly reduced the liver weight but without effects on body weight. As a critical step of the development of NAFLD, hepatic fibrosis was induced in the mice fed with HFD, shown by upregulating the expression of connective tissue growth factor and transforming growth factor beta 1, which were significantly attenuated by BL153 in a dose-dependent manner. Mechanism study revealed that BL153 significantly suppressed HFD induced hepatic lipid accumulation and oxidative stress and slightly prevented liver inflammation. These results suggest that HFD induced fibrosis in the liver can be prevented partially by BL153, probably due to reduction of hepatic lipid accumulation, inflammation and oxidative stress.