Epigallocatechin-3-Gallate attenuates lipopolysacharide-induced pneumonia via modification of inflammation, oxidative stress, apoptosis, and autophagy

• Published in: BMC complementary and alternative medicine 2024-04, Vol.24 (1), p.147-147, Article 147
• Main Authors: Shen, Meili, You, Yuting, Xu, Chengna, Chen, Zhixu
• Format: Article
• Language: English
• Subjects: Aetiology; Analysis; Animal models; Animals; Antioxidants; Apoptosis; Autophagy; Bacterial pneumonia; BAX protein; Bcl-2 protein; bcl-2-Associated X Protein - metabolism; Bronchus; caspases; Catechin; Catechin - analogs & derivatives; Cell death; Cell number; complement; Development and progression; disease progression; Enzymes; Epigallocatechin gallate; etiology; Inflammation; Inflammation - drug therapy; Inflammation - metabolism; interleukin-6; Laboratory animals; Lavage; Lipopolysaccharides; Lipopolysaccharides - toxicity; lungs; Male; males; Oxidative Stress; oxidative toxicity; Pathogens; Pneumonia; Pneumonia - drug therapy; Proteins; Rats; Rats, Wistar; Therapy; TOR protein; Tumor necrosis factor-TNF; Tumor necrosis factor-α
• ISSN: 2662-7671; 2662-7671; 1472-6882
• DOI: 10.1186/s12906-024-04436-y

Pneumonia, the acute inflammation of lung tissue, is multi-factorial in etiology. Hence, continuous studies are conducted to determine the mechanisms involved in the progression of the disease and subsequently suggest effective treatment. The present study attempted to evaluate the effects of Epigallocatechin-3-Gallate (EGCG), an herbal antioxidant, on inflammation, oxidative stress, apoptosis, and autophagy in a rat pneumonia model. Forty male Wistar rats, 5 months old and 250-290 g were divided into four groups including control, EGCG, experimental pneumonia (i/p LPS injection, 1 mg/kg), and experimental pneumonia treated with EGCG (i/p, 15 mg/kg, 1 h before and 3 h after LPS instillation). Total cell number in the bronchoalveolar lavage fluid, inflammation (TNF-a, Il-6, IL-1β, and NO), oxidative stress (Nrf2, HO-1, SOD, CAT, GSH, GPX, MDA, and TAC), apoptosis (BCL-2, BAX, CASP-3 and CASP-9), and autophagy (mTOR, LC3, BECN1) were evaluated. The findings demonstrated that EGCG suppresses the LPS-induced activation of inflammatory pathways by a significant reduction of inflammatory markers (p-value