Anti-inflammatory effects of Gingerenone A through modulation of toll-like receptor signaling pathways

Eur J Pharmacol. 2024 Nov 15:983:176997. doi: 10.1016/j.ejphar.2024.176997. Epub 2024 Sep 11.

Abstract

Toll-like receptors (TLRs) play a pivotal role in initiating immune responses, particularly in the context of inflammation. However, an excessive inflammation can detrimentally affect the immune homeostasis Thus, it is important to regulate TLR signaling pathways appropriately. Gingerenone A (GIA), a bioactive compound derived from ginger, has garnered significant attention due to its potential anti-inflammatory properties. In this study, we investigate modulatory effects of GIA on TLR signaling pathways. Results showed that GIA effectively suppressed TLR-mediated inflammatory responses by modulating key signaling molecules such as nuclear factor kappa B and interferon regulatory factor 3. These results indicate that GIA is a novel regulator of TLR signaling, offering promising avenues for the development of new anti-inflammatory agents.

Keywords: Anti-inflammation; Gingerenone A; MyD88-dependent pathway; TRIF-Dependent pathway; Toll-like receptor signaling.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents* / pharmacology
  • Humans
  • Inflammation / drug therapy
  • Inflammation / metabolism
  • Interferon Regulatory Factor-3 / metabolism
  • Lipopolysaccharides / pharmacology
  • Mice
  • NF-kappa B* / metabolism
  • RAW 264.7 Cells
  • Signal Transduction* / drug effects
  • Toll-Like Receptors* / metabolism

Substances

  • Toll-Like Receptors
  • Anti-Inflammatory Agents
  • NF-kappa B
  • Interferon Regulatory Factor-3
  • Lipopolysaccharides