Epigallocatechin-3-gallate augments antioxidant activities and inhibits inflammation during bleomycin-induced experimental pulmonary fibrosis through Nrf2–Keap1 signaling

Abstract The mechanism involved in the enhancement of antioxidant activities and resolved inflammation after epigallocatechin-3-gallate (EGCG) treatment during bleomycin-induced pulmonary fibrosis is investigated in this study. The levels of reactive-oxygen species (ROS), lipid peroxidation (LPO), h...

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Published inPulmonary pharmacology & therapeutics Vol. 22; no. 3; pp. 221 - 236
Main Authors Sriram, Narayanan, Kalayarasan, Srinivasan, Sudhandiran, Ganapasam
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.06.2009
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Abstract Abstract The mechanism involved in the enhancement of antioxidant activities and resolved inflammation after epigallocatechin-3-gallate (EGCG) treatment during bleomycin-induced pulmonary fibrosis is investigated in this study. The levels of reactive-oxygen species (ROS), lipid peroxidation (LPO), hydroxyproline and the activity of myeloperoxidase (MPO) were increased due to bleomycin challenge and were brought back to near normal status on EGCG supplementation. The decreased antioxidant status due to bleomycin challenge was also restored upon EGCG treatment. Bleomycin-induced rats showed increased cell counts as compared to control and EGCG-treated rats. Histopathological analysis showed increased inflammation and alveolar damage, while picrosirius red staining showed an increased collagen deposition in bleomycin-challenged rats that were decreased upon EGCG treatment. Immunohistochemical, immunofluorescent and immunoblot studies revealed that EGCG supplementation decreased the levels of nuclear factor-κB (NF-κB), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), which were increased upon bleomycin induction. The declined activities of Phase II enzymes such as glutathione- S -transferase (GST) and NAD(P)H:quinone oxidoreductase 1 (NQO1) in bleomycin-injured rats were restored upon EGCG treatment. Confocal microscopy, immunoblot and RT-PCR studies confirm that EGCG is a potent inducer of NF-E2-related factor 2 (Nrf2). Expression of Kelch like ECH-associated protein (Keap)-1, a vital factor in Nrf2 signaling cascade was analyzed by immunoblotting. However, there was no significant change in the expression of Keap1 in control and experimental groups. This study demonstrates the involvement of Nrf2–Keap1 signaling through which EGCG enhances antioxidant activities and Phase II enzymes with subsequent restraint inflammation during bleomycin-induced pulmonary fibrosis.
AbstractList The mechanism involved in the enhancement of antioxidant activities and resolved inflammation after epigallocatechin-3-gallate (EGCG) treatment during bleomycin-induced pulmonary fibrosis is investigated in this study. The levels of reactive-oxygen species (ROS), lipid peroxidation (LPO), hydroxyproline and the activity of myeloperoxidase (MPO) were increased due to bleomycin challenge and were brought back to near normal status on EGCG supplementation. The decreased antioxidant status due to bleomycin challenge was also restored upon EGCG treatment. Bleomycin-induced rats showed increased cell counts as compared to control and EGCG-treated rats. Histopathological analysis showed increased inflammation and alveolar damage, while picrosirius red staining showed an increased collagen deposition in bleomycin-challenged rats that were decreased upon EGCG treatment. Immunohistochemical, immunofluorescent and immunoblot studies revealed that EGCG supplementation decreased the levels of nuclear factor-κB (NF-κB), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), which were increased upon bleomycin induction. The declined activities of Phase II enzymes such as glutathione- S-transferase (GST) and NAD(P)H:quinone oxidoreductase 1 (NQO1) in bleomycin-injured rats were restored upon EGCG treatment. Confocal microscopy, immunoblot and RT-PCR studies confirm that EGCG is a potent inducer of NF-E2-related factor 2 (Nrf2). Expression of Kelch like ECH-associated protein (Keap)-1, a vital factor in Nrf2 signaling cascade was analyzed by immunoblotting. However, there was no significant change in the expression of Keap1 in control and experimental groups. This study demonstrates the involvement of Nrf2–Keap1 signaling through which EGCG enhances antioxidant activities and Phase II enzymes with subsequent restraint inflammation during bleomycin-induced pulmonary fibrosis.
The mechanism involved in the enhancement of antioxidant activities and resolved inflammation after epigallocatechin-3-gallate (EGCG) treatment during bleomycin-induced pulmonary fibrosis is investigated in this study. The levels of reactive-oxygen species (ROS), lipid peroxidation (LPO), hydroxyproline and the activity of myeloperoxidase (MPO) were increased due to bleomycin challenge and were brought back to near normal status on EGCG supplementation. The decreased antioxidant status due to bleomycin challenge was also restored upon EGCG treatment. Bleomycin-induced rats showed increased cell counts as compared to control and EGCG-treated rats. Histopathological analysis showed increased inflammation and alveolar damage, while picrosirius red staining showed an increased collagen deposition in bleomycin-challenged rats that were decreased upon EGCG treatment. Immunohistochemical, immunofluorescent and immunoblot studies revealed that EGCG supplementation decreased the levels of nuclear factor-kappaB (NF-kappaB), tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta), which were increased upon bleomycin induction. The declined activities of Phase II enzymes such as glutathione-S-transferase (GST) and NAD(P)H:quinone oxidoreductase 1 (NQO1) in bleomycin-injured rats were restored upon EGCG treatment. Confocal microscopy, immunoblot and RT-PCR studies confirm that EGCG is a potent inducer of NF-E2-related factor 2 (Nrf2). Expression of Kelch like ECH-associated protein (Keap)-1, a vital factor in Nrf2 signaling cascade was analyzed by immunoblotting. However, there was no significant change in the expression of Keap1 in control and experimental groups. This study demonstrates the involvement of Nrf2-Keap1 signaling through which EGCG enhances antioxidant activities and Phase II enzymes with subsequent restraint inflammation during bleomycin-induced pulmonary fibrosis.
Abstract The mechanism involved in the enhancement of antioxidant activities and resolved inflammation after epigallocatechin-3-gallate (EGCG) treatment during bleomycin-induced pulmonary fibrosis is investigated in this study. The levels of reactive-oxygen species (ROS), lipid peroxidation (LPO), hydroxyproline and the activity of myeloperoxidase (MPO) were increased due to bleomycin challenge and were brought back to near normal status on EGCG supplementation. The decreased antioxidant status due to bleomycin challenge was also restored upon EGCG treatment. Bleomycin-induced rats showed increased cell counts as compared to control and EGCG-treated rats. Histopathological analysis showed increased inflammation and alveolar damage, while picrosirius red staining showed an increased collagen deposition in bleomycin-challenged rats that were decreased upon EGCG treatment. Immunohistochemical, immunofluorescent and immunoblot studies revealed that EGCG supplementation decreased the levels of nuclear factor-κB (NF-κB), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), which were increased upon bleomycin induction. The declined activities of Phase II enzymes such as glutathione- S -transferase (GST) and NAD(P)H:quinone oxidoreductase 1 (NQO1) in bleomycin-injured rats were restored upon EGCG treatment. Confocal microscopy, immunoblot and RT-PCR studies confirm that EGCG is a potent inducer of NF-E2-related factor 2 (Nrf2). Expression of Kelch like ECH-associated protein (Keap)-1, a vital factor in Nrf2 signaling cascade was analyzed by immunoblotting. However, there was no significant change in the expression of Keap1 in control and experimental groups. This study demonstrates the involvement of Nrf2–Keap1 signaling through which EGCG enhances antioxidant activities and Phase II enzymes with subsequent restraint inflammation during bleomycin-induced pulmonary fibrosis.
Author Kalayarasan, Srinivasan
Sudhandiran, Ganapasam
Sriram, Narayanan
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/19138753$$D View this record in MEDLINE/PubMed
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Keywords Keap1
Inflammation
Bleomycin
Pulmonary fibrosis
Nrf2
EGCG
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Snippet Abstract The mechanism involved in the enhancement of antioxidant activities and resolved inflammation after epigallocatechin-3-gallate (EGCG) treatment during...
The mechanism involved in the enhancement of antioxidant activities and resolved inflammation after epigallocatechin-3-gallate (EGCG) treatment during...
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SubjectTerms Animals
Anti-Inflammatory Agents
Antimetabolites, Antineoplastic
Antioxidants - metabolism
Antioxidants - pharmacology
Bleomycin
Blotting, Western
Bronchoalveolar Lavage Fluid - cytology
Catechin - analogs & derivatives
Catechin - pharmacology
Collagen - metabolism
EGCG
Fluorescent Antibody Technique
Immunohistochemistry
Inflammation
Interleukin-1beta - metabolism
Intracellular Signaling Peptides and Proteins
Keap1
Kelch-Like ECH-Associated Protein 1
Lung - pathology
Male
Mast Cells - drug effects
Medical Education
Microscopy, Confocal
Nrf2
Proteins - physiology
Pulmonary fibrosis
Pulmonary Fibrosis - chemically induced
Pulmonary Fibrosis - drug therapy
Pulmonary Fibrosis - pathology
Pulmonary/Respiratory
Rats
Rats, Wistar
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction - drug effects
Title Epigallocatechin-3-gallate augments antioxidant activities and inhibits inflammation during bleomycin-induced experimental pulmonary fibrosis through Nrf2–Keap1 signaling
URI https://www.clinicalkey.es/playcontent/1-s2.0-S1094553908001363
https://dx.doi.org/10.1016/j.pupt.2008.12.010
https://www.ncbi.nlm.nih.gov/pubmed/19138753
Volume 22
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