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

IF 2.8 3区医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Biochemical and Molecular Toxicology Pub Date : 2026-03-12 DOI:10.1002/jbt.70776

Onur Unal, Halil Asci, Esma Selcuk, Adem Milletsever, Muhammet Yusuf Tepebasi, Yaren Asci, Abdurrahman Gulal, Ozlem Ozmen

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Abstract

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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没食子酸通过调节氧化应激：AKT1/NRF2和IL-10信号传导对lps诱导的肺损伤的保护作用。

本研究探讨没食子酸（GA）对脂多糖（LPS）诱导的急性肺损伤（ALI）的保护作用，通过组织病理学、免疫组织化学和遗传学评估，重点关注炎症因子和屏障完整性标志物。将32只成年雄性Wistar Albino大鼠分为对照组、LPS组、LPS + GA组和GA组。治疗组给予LPS （5 mg/kg，腹腔注射）诱导ALI和GA （100 mg/kg，腹腔注射）。LPS引起出血、肺泡间隔增厚、炎症细胞浸润和充血。白细胞介素(IL)-1β、IL-6、IL- 17a和糖原合成酶激酶-3 β (GSK3β)升高，而IL-10、水通道蛋白2 （AQP2）、闭塞带1 （ZO-1）、claudin5 （claudin5）、丝氨酸/苏氨酸激酶1 （AKT1）和核因子红细胞2相关因子2 （NRF2）降低。GA减少组织损伤和促炎细胞因子，同时恢复AKT1、NRF2、AQP2、ZO-1和clu -5。这些发现表明，GA可以减轻lps诱导的肺损伤，并与炎症和抗氧化相关信号的调节有关，包括IL-10-AKT1/GSK3β/NRF2轴的成分。

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来源期刊

Journal of Biochemical and Molecular Toxicology 生物-毒理学

CiteScore

5.80

自引率

2.80%

发文量

277

审稿时长

6-12 weeks

期刊介绍： The Journal of Biochemical and Molecular Toxicology is an international journal that contains original research papers, rapid communications, mini-reviews, and book reviews, all focusing on the molecular mechanisms of action and detoxication of exogenous and endogenous chemicals and toxic agents. The scope includes effects on the organism at all stages of development, on organ systems, tissues, and cells as well as on enzymes, receptors, hormones, and genes. The biochemical and molecular aspects of uptake, transport, storage, excretion, lactivation and detoxication of drugs, agricultural, industrial and environmental chemicals, natural products and food additives are all subjects suitable for publication. Of particular interest are aspects of molecular biology related to biochemical toxicology. These include studies of the expression of genes related to detoxication and activation enzymes, toxicants with modes of action involving effects on nucleic acids, gene expression and protein synthesis, and the toxicity of products derived from biotechnology.