Mitigating LPS-Induced Inflammation in AGS Cells via the TLR۴ Pathway with Fumaric Acids

The study investigates the effects of fumaric acid on Toll-like receptor (TLR) expression, cytokine production, and cell viability in AGS cells exposed to lipopolysaccharide (LPS), a potent inducer of inflammation. TLRs play a key role in the innate immune system, responding to pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) by producing pro-inflammatory cytokines. Fumaric acid, present in fruits and vegetables, is known for its anti-inflammatory and potential anti-cancer properties.Results indicate that LPS boosts TLR expression and the production of pro-inflammatory cytokines (IL-۱β and TNF-alpha) in AGS cells. Fumaric acid, especially at higher doses, moderates cytokine expression. Gene expression analysis suggests fumaric acid may alleviate inflammation by affecting cytokine production, possibly aiding cancer treatment.Annexin PI assay shows fumaric acid's independent impact on AGS cell viability; in combination with LPS, it significantly alters cell death, implying synergistic interaction. MTT assay further confirms fumaric acid's positive effect on AGS cell survival against LPS-induced damage.The discussion highlights fumaric acid's known anti-inflammatory and anti-cancer effects. This study adds insights into its impact on cytokine production and safeguarding cells from LPS damage. The differing effects on viability and death when fumaric acid and LPS are combined require further exploration considering factors like cell type, dose, and exposure time. To conclude, this research underscores fumaric acid's therapeutic potential against inflammation and cancer. It reveals its influence on TLR signaling, cytokine production, and cell viability in AGS cells exposed to LPS. Nevertheless, more research is needed to fully understand its mechanisms and clinical uses.

کلیدواژه ها:

Fumaric acid ، Inflammation ، Gastric Cancer ، Pattern recognition receptors ، lipopolysaccharide