Norbergenin prevents LPS-induced inflammatory responses in macrophages through inhibiting NFkB, MAPK and STAT3 activation and blocking metabolic reprogramming
Ontology highlight
ABSTRACT: Inflammation is thought to be a key cause of many chronic diseases and cancer. However, current therapeutic agents to control inflammation have limited long-term use potential due to various side-effects. This study aimed to examine norbergenin, a constituent of traditional anti-inflammatory recipes, on LPS-induced proinflammatory signaling in macrophages and elucidate the underlying mechanisms by integrative metabolomics and proteomics platforms. We found that LPS-induced production of NO, IL1β, TNFα, IL6 and iNOS in macrophages was alleviated by norbergenin via suppressed activation of TLR2 mediated NFkB, MAPKs and STAT3 signaling pathways. In addition, norbergenin was capable of overcoming LPS-triggered metabolic reprogramming in macrophages and restrained the facilitated glycolysis, promoted the reduced OXPHOS, and restored the aberrant metabolites within the TCA cycle. This is linked to its modulation of metabolic enzymes to support its anti-inflammatory activity. Thus, our results uncover that norbergenin regulates inflammatory signaling cascades and metabolic reprogramming in LPS stimulated macrophages to exert its anti-inflammatory potential.
INSTRUMENT(S): Gas Chromatography MS -, Liquid Chromatography MS - positive - reverse phase
SUBMITTER: Zhengnan Cai
PROVIDER: MTBLS7127 | MetaboLights | 2023-04-06
REPOSITORIES: MetaboLights
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The resolution of
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Dunster JL, Byrne HM, King JR.
Bull. Math. Biol. 2014 Aug; 76(8):
1953-1980
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There is growing interest in inflammation due to its
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This model is hosted on
BioModels Database
and identified by:
BIOMD0000000616.
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To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
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