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

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 Epigal...

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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
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description 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 
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The findings demonstrated that EGCG suppresses the LPS-induced activation of inflammatory pathways by a significant reduction of inflammatory markers (p-value &lt; 0.001). In addition, the upregulation of BCL-2 and downregulation of BAX and caspases revealed that EGCG suppressed LPS-induced apoptosis. Furthermore, ECGC suppressed oxidative injury while promoting autophagy in rats with pneumonia (p-value &lt; 0.05). 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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
title Epigallocatechin-3-Gallate attenuates lipopolysacharide-induced pneumonia via modification of inflammation, oxidative stress, apoptosis, and autophagy
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