Mechanistic Insights into Isorhamnetin: Targeting MAPK and NF-κB Pathways to Mitigate LPS-Induced Inflammation.

Introduction Chronic inflammation may result in mucosal damage, presenting as pain, edema, convulsions, and fever symptoms. This study investigated the anti-inflammatory characteristics of isorhamnetin (ISO) and its potential as a medicinal agent. Method In this study, in vitro tests were performed in which macrophages were activated with lipopolysaccharide (LPS) to evaluate the effect of ISO on inflammation. We concentrated on quantifying the synthesis of pro-inflammatory cytokines, interleukin [IL]-1β, IL-6, and tumor necrosis factor [TNF-α], as well as mediators, such as nitric oxide [NO] and prostaglandin E2 [PGE2], in LPS-stimulated RAW 264.7 cells. Results The findings indicated that ISO significantly decreased levels of NO and PGE2 while maintaining cellular integrity. ISO reduced the synthesis of pro-inflammatory cytokines in a dose-dependent manner. Moreover, ISO treatment decreased mRNA levels of inducible nitric oxide synthase [iNOS] and cyclooxygenase-2 [COX-2], which were enhanced following LPS exposure. Mechanistic investigations revealed that the antiinflammatory properties of ISO were facilitated by the inhibition of phosphorylation in the mitogen-activated protein kinase [MAPK] family and the downregulation of nuclear factor-kappa B inhibitor [IκB-α] within both the MAPK and nuclear factor-kappa B [NF-κB] pathways. Conclusion These findings establish ISO as a viable alternative for treating inflammatory diseases by specifically inhibiting essential inflammatory pathways.