Gallic acid attenuates LPS-induced inflammation in Caco-2 cells by suppressing the activation of the NF-κB/MAPK signaling pathway

• Gallic acid (GA) restores LPS-induced downregulation of tight junction proteins (Claudin-1, Occludin, ZO-1) and reduces inflammatory cytokines (IL-6, IL-1β, TNF-α) in Caco-2 cells. • GA exerts anti-apoptotic effects by decreasing pro-apoptotic factors (Bax, Bad, Caspase-3/8/9) and increasing anti-apoptotic Bcl-2, while also mitigating oxidative stress via ROS reduction and antioxidant enzyme restoration. • The anti-inflammatory mechanism of GA involves suppression of NF-κB/MAPK signaling pathway activation, specifically inhibiting phosphorylation of p65, IκB-α, p38, JNK, and ERK. • These findings suggest GA as a promising therapeutic candidate for intestinal inflammation and IBD, warranting further in vivo validation and clinical exploration.