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Preclinical analysis shows Gallic Acid reduces inflammation and oxidative stress in lung injury, suggesting therapeutic potential.
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.
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Ünal et al. (2026) studied this question.
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