Protective Effects of Gallic Acid in LPS‐Induced Lung Injury via Modulation of Oxidative Stress: AKT1/NRF2 and IL‐10 Signaling

This study investigated the protective effects of Gallic acid (GA) on Lipopolysaccharide (LPS)-induced acute lung injury (ALI), focusing on inflammatory cytokines and barrier integrity markers through histopathological, immunohistochemical, and genetic evaluations. Thirty-two adult male Wistar Albino rats were divided into Control, LPS, LPS + GA, and GA groups. LPS (5 mg/kg, intraperitoneal) induced ALI and GA (100 mg/kg, intraperitoneal) was administered to the treatment group. LPS caused hemorrhage, interalveolar septa thickening, inflammatory cell infiltration, and hyperemia. Interleukin (IL)-1β, IL-6, IL-17A, and glycogen synthase kinase-3 beta (GSK3β) increased, while IL-10, aquaporin 2 (AQP2), zonula occludens 1 (ZO-1), claudin 5 (Clau-5), serine/threonine kinase 1 (AKT1), and nuclear factor erythroid 2-related factor 2 (NRF2) decreased. GA reduced tissue damage and pro-inflammatory cytokines while restoring AKT1, NRF2, AQP2, ZO-1, and Clau-5. These findings suggest that GA attenuates LPS-induced lung injury and is associated with modulation of inflammatory and antioxidant-related signaling, including components of the IL-10-AKT1/GSK3β/NRF2 axis.