Glucosinolates Extracts from Brassica juncea Ameliorate HFD-Induced Non-Alcoholic Steatohepatitis

Author:

Sheu Ming-Jen1,Yeh Mei-Chen2,Tsai Ming-Chang345,Wang Chi-Chih345ORCID,Chang Yen-Ling3,Wang Chau-Jong67,Huang Hui-Pei78

Affiliation:

1. Division of Hepatogastroenterology, Department of Internal Medicine, Chi Mei Medical Center, No. 901, Zhonghua Rd. Yongkang Dist., Tainan City 71004, Taiwan

2. Division of Metabolism and Endocrinology, Department of Internal Medicine, Chi Mei Medical Center, Tainan 71004, Taiwan

3. Institute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan

4. School of Medicine, Chung Shan Medical University, Taichung 402, Taiwan

5. Division of Gastroenterology and Hepatology, Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung 402, Taiwan

6. Department of Health Industry Technology Management, Chung Shan Medical University, Taichung 402, Taiwan

7. Department of Medical Research, Chung Shan Medical University Hospital, Taichung 402, Taiwan

8. Department of Biochemistry, School of Medicine, Chung Shan Medical University, Taichung 40242, Taiwan

Abstract

Non-alcoholic fatty liver disease (NAFLD) is mainly characterized by excessive fat accumulation in the liver. It spans a spectrum of diseases from hepatic steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Brassica juncea is rich in glucosinolates and has been proven to possess many potential pharmacological properties, including hypoglycemic, anti-oxidation, anti-inflammatory, and anti-carcinogenic activities. This study aims to investigate whether whole-plant Brassica juncea (WBJ) and its glucosinolates extracts (BGE) have hepatoprotective effects against a high-fat diet (HFD)-induced NAFLD and further explore the mechanism underlying this process in vivo and in vitro. WBJ treatment significantly reduced body fat, dyslipidemia, hepatic steatosis, liver injury, and inflammation; WBJ treatment also reversed the antioxidant enzyme activity to attenuate oxidative stress in HFD-fed rat liver. Moreover, WBJ and BGE enhanced the activation of AMPK to reduce SREBPs, fatty acid synthase, and HMG-CoA reductase but increased the expression of CPT-I and PPARα to improve hepatic steatosis. In addition, WBJ and BGE could ameliorate NAFLD by inhibiting TNF-α and NF-κB. Based on the above results, this study demonstrates that WBJ and BGE ameliorate HFD-induced hepatic steatosis and liver injury. Therefore, these treatments could represent an unprecedented hope toward improved strategies for NAFLD.

Funder

Chung Shan Medical University

Chi Mei Medical Center

Publisher

MDPI AG

Subject

Food Science,Nutrition and Dietetics

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