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

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...

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Main Authors: Jian Wang, Chi Zhang, Zhiguo Zhang, Qiang Chen, Xuemian Lu, Minglong Shao, Liangmiao Chen, Hong Yang, Fangfang Zhang, Peng Cheng, Yi Tan, Ki-Soo Kim, Ki Ho Kim, Bochu Wang, Young Heui Kim
Format: Article
Language:English
Published: Hindawi Limited 2014-01-01
Series:Oxidative Medicine and Cellular Longevity
Online Access:http://dx.doi.org/10.1155/2014/674690
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language English
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author Jian Wang
Chi Zhang
Zhiguo Zhang
Qiang Chen
Xuemian Lu
Minglong Shao
Liangmiao Chen
Hong Yang
Fangfang Zhang
Peng Cheng
Yi Tan
Ki-Soo Kim
Ki Ho Kim
Bochu Wang
Young Heui Kim
spellingShingle Jian Wang
Chi Zhang
Zhiguo Zhang
Qiang Chen
Xuemian Lu
Minglong Shao
Liangmiao Chen
Hong Yang
Fangfang Zhang
Peng Cheng
Yi Tan
Ki-Soo Kim
Ki Ho Kim
Bochu Wang
Young Heui Kim
BL153 Partially Prevents High-Fat Diet Induced Liver Damage Probably via Inhibition of Lipid Accumulation, Inflammation, and Oxidative Stress
Oxidative Medicine and Cellular Longevity
author_facet Jian Wang
Chi Zhang
Zhiguo Zhang
Qiang Chen
Xuemian Lu
Minglong Shao
Liangmiao Chen
Hong Yang
Fangfang Zhang
Peng Cheng
Yi Tan
Ki-Soo Kim
Ki Ho Kim
Bochu Wang
Young Heui Kim
author_sort Jian Wang
title BL153 Partially Prevents High-Fat Diet Induced Liver Damage Probably via Inhibition of Lipid Accumulation, Inflammation, and Oxidative Stress
title_short BL153 Partially Prevents High-Fat Diet Induced Liver Damage Probably via Inhibition of Lipid Accumulation, Inflammation, and Oxidative Stress
title_full BL153 Partially Prevents High-Fat Diet Induced Liver Damage Probably via Inhibition of Lipid Accumulation, Inflammation, and Oxidative Stress
title_fullStr BL153 Partially Prevents High-Fat Diet Induced Liver Damage Probably via Inhibition of Lipid Accumulation, Inflammation, and Oxidative Stress
title_full_unstemmed BL153 Partially Prevents High-Fat Diet Induced Liver Damage Probably via Inhibition of Lipid Accumulation, Inflammation, and Oxidative Stress
title_sort bl153 partially prevents high-fat diet induced liver damage probably via inhibition of lipid accumulation, inflammation, and oxidative stress
publisher Hindawi Limited
series Oxidative Medicine and Cellular Longevity
issn 1942-0900
1942-0994
publishDate 2014-01-01
description 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.
url http://dx.doi.org/10.1155/2014/674690
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spelling doaj-1403b31c418746c38449241c71abf21a2020-11-24T22:16:41ZengHindawi LimitedOxidative Medicine and Cellular Longevity1942-09001942-09942014-01-01201410.1155/2014/674690674690BL153 Partially Prevents High-Fat Diet Induced Liver Damage Probably via Inhibition of Lipid Accumulation, Inflammation, and Oxidative StressJian Wang0Chi Zhang1Zhiguo Zhang2Qiang Chen3Xuemian Lu4Minglong Shao5Liangmiao Chen6Hong Yang7Fangfang Zhang8Peng Cheng9Yi Tan10Ki-Soo Kim11Ki Ho Kim12Bochu Wang13Young Heui Kim14College of Bioengineering, Chongqing University, Chongqing 400044, ChinaThe Chinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences & Key Laboratory of Biotechnology Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, ChinaDepartment of Pediatrics of the University of Louisville, The Kosair Children’s Hospital Research Institute, Louisville, KY 20202, USADepartment of Pediatrics of the University of Louisville, The Kosair Children’s Hospital Research Institute, Louisville, KY 20202, USAThe Chinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences & Key Laboratory of Biotechnology Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, ChinaThe Chinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences & Key Laboratory of Biotechnology Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, ChinaThe Chinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences & Key Laboratory of Biotechnology Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, ChinaThe Chinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences & Key Laboratory of Biotechnology Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, ChinaThe Chinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences & Key Laboratory of Biotechnology Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, ChinaThe Chinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences & Key Laboratory of Biotechnology Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, ChinaThe Chinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences & Key Laboratory of Biotechnology Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, ChinaBioland Biotec Co., Ltd., Zhangjiang Modern Medical Device Park, Pudong, Shanghai 201201, ChinaBioland R&D Center, 59 Songjeongni 2-gil, Byeongcheon, Dongnam, Cheonan, Chungnam 330-863, Republic of KoreaCollege of Bioengineering, Chongqing University, Chongqing 400044, ChinaBioland R&D Center, 59 Songjeongni 2-gil, Byeongcheon, Dongnam, Cheonan, Chungnam 330-863, Republic of KoreaThe 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.http://dx.doi.org/10.1155/2014/674690