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. 2022 Jan 19;12:818227. doi: 10.3389/fphar.2021.818227

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Copyright © 2022 He, Hu, Liu, Zhu, Zhang, You, Shao, Li, Zhang, Cui, He, Ge and Yang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Proposed mechanism of POL and its main active component myricetin in treating NASH through inhibiting PTGS2. In macrophages, POL and myricetin could decrease the secretion of inflammatory mediators such as IL-6, IL-1β, and TNF-α through down-regulating PTGS2. In hepatocytes, POL and myricetin could regulate lipid synthesis and homostasis by down-regulating FASN, SREBP1c, and SCD1 and up-regulating ACC1 and CPT1a through inhibiting PTGS2. Thus, POL could reduce lipid accumulation of hepatocyte and inhibit hepatic inflammation to treat NASH.