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Article

Astaxanthin Prevents Diet-Induced NASH Progression by Shaping Intrahepatic Immunity

1
Department of Surgery, University of Missouri, Columbia, MO 65212, USA
2
Harry S. Truman Memorial VA Hospital, Columbia, MO 65201, USA
3
Department of Molecular Microbiology and Immunology, University of Missouri, Columbia, MO 65212, USA
*
Authors to whom correspondence should be addressed.
Academic Editor: Takemi Akahane
Int. J. Mol. Sci. 2021, 22(20), 11037; https://doi.org/10.3390/ijms222011037
Received: 9 September 2021 / Revised: 8 October 2021 / Accepted: 11 October 2021 / Published: 13 October 2021
(This article belongs to the Special Issue Liver–Gut Axis 2.0)
Dietary change leads to a precipitous increase in non-alcoholic fatty liver disease (NAFLD) from simple steatosis to the advanced form of non-alcoholic steatohepatitis (NASH), affecting approximately 25% of the global population. Although significant efforts greatly advance progress in clarifying the pathogenesis of NAFLD and identifying therapeutic targets, no therapeutic agent has been approved. Astaxanthin (ASTN), a natural antioxidant product, exerts an anti-inflammation and anti-fibrotic effect in mice induced with carbon tetrachloride (CCl4) and bile duct ligation (BDL); thus, we proposed to further investigate the potential effect of ASTN on a diet-induced mouse NASH and liver fibrosis, as well as the underlying cellular and molecular mechanisms. By treating pre-development of NASH in mice induced with a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD), we have demonstrated that oral administration ASTN preventively ameliorated NASH development and liver fibrosis by modulating the hepatic immune response, liver inflammation, and oxidative stress. Specifically, ASTN treatment led to the reduction in liver infiltration of monocyte-derived macrophages, hepatic stellate cell (HSC) activation, oxidative stress response, and hepatocyte death, accompanied by the decreased hepatic gene expression of proinflammatory cytokines such as TNF-α, TGF-β1, and IL-1β. In vitro studies also demonstrated that ASTN significantly inhibited the expression of proinflammatory cytokines and chemokine CCL2 in macrophages in response to lipopolysaccharide (LPS) stimulation. Overall, in vivo and in vitro studies suggest that ASTN functions as a promising therapeutic agent to suppress NASH and liver fibrosis via modulating intrahepatic immunity. View Full-Text
Keywords: non-alcoholic fatty liver disease; non-alcoholic steatohepatitis; astaxanthin; intrahepatic immune response; treatment; nanoparticles non-alcoholic fatty liver disease; non-alcoholic steatohepatitis; astaxanthin; intrahepatic immune response; treatment; nanoparticles
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MDPI and ACS Style

Yang, M.; Kimchi, E.T.; Staveley-O’Carroll, K.F.; Li, G. Astaxanthin Prevents Diet-Induced NASH Progression by Shaping Intrahepatic Immunity. Int. J. Mol. Sci. 2021, 22, 11037. https://doi.org/10.3390/ijms222011037

AMA Style

Yang M, Kimchi ET, Staveley-O’Carroll KF, Li G. Astaxanthin Prevents Diet-Induced NASH Progression by Shaping Intrahepatic Immunity. International Journal of Molecular Sciences. 2021; 22(20):11037. https://doi.org/10.3390/ijms222011037

Chicago/Turabian Style

Yang, Ming, Eric T. Kimchi, Kevin F. Staveley-O’Carroll, and Guangfu Li. 2021. "Astaxanthin Prevents Diet-Induced NASH Progression by Shaping Intrahepatic Immunity" International Journal of Molecular Sciences 22, no. 20: 11037. https://doi.org/10.3390/ijms222011037

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