Glucosinolates Extracts from Brassica juncea Ameliorate HFD-Induced Non-Alcoholic Steatohepatitis.
Ming-Jen SheuMei-Chen YehMing-Chang TsaiChi-Chih WangYen-Ling ChangChau-Jong WangHui-Pei HuangPublished in: Nutrients (2023)
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.
Keyphrases
- liver injury
- drug induced
- high fat diet
- oxidative stress
- diabetic rats
- adipose tissue
- insulin resistance
- fatty acid
- anti inflammatory
- high glucose
- signaling pathway
- liver fibrosis
- poor prognosis
- induced apoptosis
- dna damage
- endothelial cells
- ischemia reperfusion injury
- arabidopsis thaliana
- replacement therapy
- inflammatory response
- cell proliferation
- nuclear factor
- smoking cessation
- genome wide identification
- human health