Naringenin inhibits pro‑inflammatory cytokine production in macrophages through inducing MT1G to suppress the activation of NF‑κB. (September 2021)

• Record Type: Journal Article
• Authors: Yang, Jie; Liu, Lin; Li, Mengmeng; Huang, Xuemei; Yang, Huanjie; Li, Kai
• Is Part Of: Molecular immunology. Volume 137(2021)
• Page Start: 155
• Page End: 162
• Publication Date: 2021-09
• Subjects: Naringenin -- Inflammation -- MT1G -- NF-κB; Immunochemistry -- Periodicals; Molecular biology -- Periodicals; Immunochemistry -- Periodicals; Allergy and Immunology -- Periodicals; Molecular Biology -- Periodicals; Immunochimie -- Périodiques; Biologie moléculaire -- Périodiques; Immunochemistry; Molecular biology; Periodicals; Electronic journals; 571.96
• DOI: 10.1016/j.molimm.2021.07.003
• Languages: English
• ISSNs: 0161-5890

Abstract

Highlights: Naringenin suppresses LPS-induced pro‑inflammatory cytokine production in macrophages. Nar-mediated inhibition of pro-inflammatory cytokines expression is dependent on MT1G. MT1G acts as zinc chelator to represses NF-κB activation and LPS-induced pro-inflammatory cytokines expression. Abstract: Naringenin (Nar) is a flavanone that has been suggested to provide human health benefits such as anti-inflammatory, anti-oxidant and anti-cancer properties. However, the mechanisms underlying these benefits are complex and still not fully understood. In this study, we investigated the effect of Nar on the inflammatory response of macrophages and its underlying mechanism. In lipopolysaccharide (LPS)-stimulated human macrophages, Nar inhibited the activation of NF-κB pathway and suppressed the downstream expression of pro-inflammatory factors. In addition, Nar was also able to induce metallothionein 1 G (MT1G) expression, and the inhibitory effects of Nar on the production of pro-inflammatory cytokines was dependent on MT1G. Mechanistically, we found that MT1G-mediated inhibition of pro-inflammatory cytokines responses might be through repressing NF-κB activation via zinc chelation. Overall, this study reveals a novel mechanism of Nar on inflammatory responses, the suppression of NF-κB activation through upregulation of MT1G.