Abstract Title:

Astaxanthin attenuates hepatic damages and mitochondrial dysfunction in nonalcoholic fatty liver disease by up-regulating the FGF21/PGC-1α pathway.

Abstract Source:

Br J Pharmacol. 2020 May 22. Epub 2020 May 22. PMID: 32446270

Abstract Author(s):

Liwei Wu, Wenhui Mo, Jiao Feng, Jingjing Li, Qiang Yu, Sainan Li, Jie Zhang, Kan Chen, Jie Ji, Weiqi Dai, Jianye Wu, Xuanfu Xu, Yuqing Mao, Chuanyong Guo

Article Affiliation:

Liwei Wu


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 type of carotenoid,and beneficial effects of Ax,including anti-oxidative, anti-inflammatory, and anti-tumor activity, have been identified. The present study aimed to elucidate the protective effect of Ax against NAFLD and its underlying mechanism.

EXPERIMENTAL APPROACH: Mice were fed either a high fat or chow diet, with or without AX, for up to 12 weeks. L02 cells were treated with free fatty acids combined with different doses of Ax for 48 h. Histopathology, expression of lipid metabolism, inflammation, apoptosis, and fibrosis-related gene expression were assessed. And the function of mitochondria were also evaluated.

KEY RESULTS: The results indicated that Ax attenuated HFD- and FFA-induced lipid accumulation and its associated oxidative stress, cell apoptosis, inflammation, and fibrosis both in vivo and in vitro. Ax upregulated FGF21 and PGC-1α expression in damaged hepatocytes, which suggested an unrecognized mechanism of Ax on ameliorating NAFLD.

CONCLUSION AND IMPLICATIONS: Ax attenuated hepatocyte damage and mitochondrial dysfunction in NAFLD by upregulating FGF21/PGC-1α pathway. Our studies verified that Ax may become a promising drug to treat or relieve NAFLD.

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