Protective Effect of Fuzi Lizhong Decoction against Non-alcoholic Fatty Liver Disease via Anti-inflammatory Response through Regulating p53 and PPARG Signaling

Fuzi Lizhong decoction (FLD) is derived from an ancient Chinese Pharmacopoeia and has been used in clinical treatment for years. The present study aimed to investigate the activities and underlying mechanisms of FLD against non-alcoholic fatty liver disease (NAFLD). Network pharmacology analysis dem...

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Bibliographic Details
Published in:Biological & pharmaceutical bulletin 2020/11/01, Vol.43(11), pp.1626-1633
Main Authors: Yang, Jiayao, Ma, Wei, Mei, Qunchao, Song, Juefei, Shu, Lei, Zhang, Shu, Li, Chenyu, An, Liu, Du, Nianlong, Shi, Zhaohong
Format: Article
Language:eng ; jpn
Subjects:
Cholesterol
Fatty liver
Fuzi Lizhong decoction
High fat diet
Immune system
inflammatory
Interleukin 10
Linoleic acid
Liver diseases
non-alcoholic fatty liver disease
Oleic acid
p53
p53 Protein
peroxisome proliferator activated receptor gamma
Peroxisome proliferator-activated receptors
α-Interferon
β-Interferon
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Summary:Fuzi Lizhong decoction (FLD) is derived from an ancient Chinese Pharmacopoeia and has been used in clinical treatment for years. The present study aimed to investigate the activities and underlying mechanisms of FLD against non-alcoholic fatty liver disease (NAFLD). Network pharmacology analysis demonstrated that FLD might affect NAFLD through regulating p53 and peroxisome proliferator activated receptor gamma (PPARG), which has been confirmed in vitro and in vivo. In vivo NAFLD was induced in rats by a high-fat diet, and in vitro studies were performed on HL-7702 cells treated with oleic acid and linoleic acid. We showed that FLD significantly improved NAFLD by regulating the immune system to induce the release of interleukin-10 (IL-10), interferon-α (IFN-α), and IFN-β through activating p53 signaling and inhibiting PPARG signaling in vivo and in vitro. P53 inhibition induced by NAFLD was recused by FLD, while PPARG overexpression induced by NAFLD was inhibited by FLD. In addition, NAFLD resulted in increased levels of total cholesterol, triglyceride, and blood glucose in the serum and free fatty acid in the liver, which were reduced by FLD treatment. Evidently, FLD exhibited potent protective effects against NAFLD via p53 and PPARG signaling. Our study could provide novel insights into the mechanisms of FLD as an anti-inflammatory candidate for the treatment of NAFLD in the future.
ISSN:0918-6158
1347-5215
DOI:10.1248/bpb.b20-00053