Liwei Wu1, Wenhui Mo2, Jiao Feng1, Jingjing Li1,3, Qiang Yu1, Sainan Li1, Jie Zhang1,4, Kan Chen1, Jie Ji1, Weiqi Dai1,3,5,6,7, Jianye Wu3, Xuanfu Xu2, Yuqing Mao8, Chuanyong Guo1. 1. Department of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China. 2. Department of Gastroenterology, Shidong Hospital of Shanghai, Shanghai, China. 3. Department of Gastroenterology, Putuo People's Hospital, Tongji University School of Medicine, Shanghai, China. 4. Shanghai Tenth Hospital, School of Clinical Medicine of Nanjing Medical University, Shanghai, China. 5. Department of Gastroenterology, Zhongshan Hospital of Fudan University, Shanghai, China. 6. Shanghai Institute of Liver Diseases, Zhongshan Hospital of Fudan University, Shanghai, China. 7. Shanghai Tongren Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China. 8. Department of Gastroenterology, Shanghai First People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Abstract
BACKGROUND AND PURPOSE: Non-alcoholic fatty liver disease (NAFLD) is considered to be one of the most common chronic liver diseases across worldwide. Astaxanthin (Ax) is a carotenoid, and beneficial effects of astaxanthin, including anti-oxidative, anti-inflammatory, and anti-tumour activity, have been identified. The present study aimed to elucidate the protective effect of astaxanthin against NAFLD and its underlying mechanism. EXPERIMENTAL APPROACH: Mice were fed either a high fat or chow diet, with or without astaxanthin, for up to 12 weeks. L02 cells were treated with free fatty acids combined with different doses of astaxanthin for 48 h. Histopathology, expression of lipid metabolism, inflammation, apoptosis, and fibrosis-related gene expression were assessed. And the function of mitochondria was also evaluated. KEY RESULTS: The results indicated that astaxanthin attenuated HFD- and FFA-induced lipid accumulation and its associated oxidative stress, cell apoptosis, inflammation, and fibrosis both in vivo and in vitro. Astaxanthin up-regulated FGF21 and PGC-1α expression in damaged hepatocytes, which suggested an unrecognized mechanism of astaxanthin on ameliorating NAFLD. CONCLUSION AND IMPLICATIONS: Astaxanthin attenuated hepatocyte damage and mitochondrial dysfunction in NAFLD by up-regulating FGF21/PGC-1α pathway. Our results suggest that astaxanthin may become a promising drug to treat or relieve NAFLD.
BACKGROUND AND PURPOSE:Non-alcoholic fatty liver disease (NAFLD) is considered to be one of the most common chronic liver diseases across worldwide. Astaxanthin (Ax) is a carotenoid, and beneficial effects of astaxanthin, including anti-oxidative, anti-inflammatory, and anti-tumour activity, have been identified. The present study aimed to elucidate the protective effect of astaxanthin against NAFLD and its underlying mechanism. EXPERIMENTAL APPROACH: Mice were fed either a high fat or chow diet, with or without astaxanthin, for up to 12 weeks. L02 cells were treated with free fatty acids combined with different doses of astaxanthin for 48 h. Histopathology, expression of lipid metabolism, inflammation, apoptosis, and fibrosis-related gene expression were assessed. And the function of mitochondria was also evaluated. KEY RESULTS: The results indicated that astaxanthin attenuated HFD- and FFA-induced lipid accumulation and its associated oxidative stress, cell apoptosis, inflammation, and fibrosis both in vivo and in vitro. Astaxanthin up-regulated FGF21 and PGC-1α expression in damaged hepatocytes, which suggested an unrecognized mechanism of astaxanthin on ameliorating NAFLD. CONCLUSION AND IMPLICATIONS: Astaxanthinattenuated hepatocyte damage and mitochondrial dysfunction in NAFLD by up-regulating FGF21/PGC-1α pathway. Our results suggest that astaxanthin may become a promising drug to treat or relieve NAFLD.
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