Epigallocatechin 3‐gallate attenuates arthritis by regulating Nrf2, HO‐1, and cytokine levels in an experimental arthritis model

Epigallocatechin 3‐gallate (EGCG) is a polyphenol that has been shown to have antioxidant and anti‐inflammatory effects. In this study, collagen‐induced arthritis (CIA) model, in Wistar albino rats, was used to elucidate the effect of EGCG on pathogenetic pathways in inflammatory arthritis. The leve...

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Veröffentlicht in:Biotechnology and applied biochemistry 2020-05, Vol.67 (3), p.317-322, Article bab.1860
Hauptverfasser: Karatas, Ahmet, Dagli, Adile Ferda, Orhan, Cemal, Gencoglu, Hasan, Ozgen, Metin, Sahin, Nurhan, Sahin, Kazim, Koca, Suleyman Serdar
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container_end_page 322
container_issue 3
container_start_page 317
container_title Biotechnology and applied biochemistry
container_volume 67
creator Karatas, Ahmet
Dagli, Adile Ferda
Orhan, Cemal
Gencoglu, Hasan
Ozgen, Metin
Sahin, Nurhan
Sahin, Kazim
Koca, Suleyman Serdar
description Epigallocatechin 3‐gallate (EGCG) is a polyphenol that has been shown to have antioxidant and anti‐inflammatory effects. In this study, collagen‐induced arthritis (CIA) model, in Wistar albino rats, was used to elucidate the effect of EGCG on pathogenetic pathways in inflammatory arthritis. The levels of serum TNF‐α, IL‐17, malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx); the expression levels of tissue heme oxygenase‐1 (HO‐1) and nuclear factor erythroid 2‐related factor 2 (Nrf2); histopathologically, perisynovial inflammation and cartilage‐bone destruction were examined. In the sham group, serum TNF‐α, IL‐17, and MDA levels increased, while SOD, CAT, GPx levels, and the expressions of Nrf2 and HO‐1 decreased. On the other hand, in the EGCG administered groups, serum TNF‐α, IL‐17, and MDA levels improved, while SOD, CAT, GPx levels and the expressions of Nrf2 and HO‐1 increased. Moreover, histopathological analysis has shown that perisynovial inflammation and cartilage‐bone destruction decreased in the EGCG administered groups. These results suggest that EGCG has an antiarthritic effect by regulating the oxidative‐antioxidant balance and cytokine levels in the CIA model, which is a surrogate experimental model of rheumatoid arthritis. EGCG applications, in experimental arthritis model, enhance the antioxidants enzyme levels and the expressions of Nrf‐2 and HO‐1. On the other hand, EGCG applications decrease the level of MDA, an oxidant, and the level of pro‐inflammatory cytokines. Moreover, EGCG ameliorates the clinical and histological findings of inflammatory arthritis.
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In this study, collagen‐induced arthritis (CIA) model, in Wistar albino rats, was used to elucidate the effect of EGCG on pathogenetic pathways in inflammatory arthritis. The levels of serum TNF‐α, IL‐17, malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx); the expression levels of tissue heme oxygenase‐1 (HO‐1) and nuclear factor erythroid 2‐related factor 2 (Nrf2); histopathologically, perisynovial inflammation and cartilage‐bone destruction were examined. In the sham group, serum TNF‐α, IL‐17, and MDA levels increased, while SOD, CAT, GPx levels, and the expressions of Nrf2 and HO‐1 decreased. On the other hand, in the EGCG administered groups, serum TNF‐α, IL‐17, and MDA levels improved, while SOD, CAT, GPx levels and the expressions of Nrf2 and HO‐1 increased. Moreover, histopathological analysis has shown that perisynovial inflammation and cartilage‐bone destruction decreased in the EGCG administered groups. These results suggest that EGCG has an antiarthritic effect by regulating the oxidative‐antioxidant balance and cytokine levels in the CIA model, which is a surrogate experimental model of rheumatoid arthritis. EGCG applications, in experimental arthritis model, enhance the antioxidants enzyme levels and the expressions of Nrf‐2 and HO‐1. On the other hand, EGCG applications decrease the level of MDA, an oxidant, and the level of pro‐inflammatory cytokines. Moreover, EGCG ameliorates the clinical and histological findings of inflammatory arthritis.</description><identifier>ISSN: 0885-4513</identifier><identifier>EISSN: 1470-8744</identifier><identifier>DOI: 10.1002/bab.1860</identifier><identifier>PMID: 31746064</identifier><language>eng</language><publisher>HOBOKEN: Wiley</publisher><subject><![CDATA[Animal models ; Animals ; Antioxidants ; Arthritis ; Arthritis, Experimental - chemically induced ; Arthritis, Experimental - drug therapy ; Arthritis, Experimental - metabolism ; Biochemistry & Molecular Biology ; Biotechnology & Applied Microbiology ; Cartilage ; Catalase ; Catechin - analogs & derivatives ; Catechin - pharmacology ; Collagen ; Collagen Type II ; collagen‐induced arthritis ; Cytokines ; Cytokines - antagonists & inhibitors ; Cytokines - biosynthesis ; Destruction ; Disease Models, Animal ; Epigallocatechin-3-gallate ; Female ; Glutathione ; Glutathione peroxidase ; Heme ; Heme Oxygenase (Decyclizing) - antagonists & inhibitors ; Heme Oxygenase (Decyclizing) - biosynthesis ; Inflammation ; Life Sciences & Biomedicine ; Malondialdehyde ; NF-E2-Related Factor 2 - antagonists & inhibitors ; NF-E2-Related Factor 2 - biosynthesis ; Oxygenase ; Peroxidase ; Rats ; Rats, Wistar ; Rheumatoid arthritis ; Science & Technology ; Superoxide dismutase ; Tumor necrosis factor]]></subject><ispartof>Biotechnology and applied biochemistry, 2020-05, Vol.67 (3), p.317-322, Article bab.1860</ispartof><rights>2019 International Union of Biochemistry and Molecular Biology, Inc.</rights><rights>2020 International Union of Biochemistry and Molecular Biology, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>29</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000555601200002</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c4150-a9a3069a250571f7dc16b0b216ffd6cb2ab89ed0c6c8318b2b06841bced3a303</citedby><cites>FETCH-LOGICAL-c4150-a9a3069a250571f7dc16b0b216ffd6cb2ab89ed0c6c8318b2b06841bced3a303</cites><orcidid>0000-0003-4995-430X ; 0000-0002-6725-4182 ; 0000-0003-4138-7689 ; 0000-0003-4077-4134 ; 0000-0001-9542-5244</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fbab.1860$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fbab.1860$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27929,27930,28253,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31746064$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Karatas, Ahmet</creatorcontrib><creatorcontrib>Dagli, Adile Ferda</creatorcontrib><creatorcontrib>Orhan, Cemal</creatorcontrib><creatorcontrib>Gencoglu, Hasan</creatorcontrib><creatorcontrib>Ozgen, Metin</creatorcontrib><creatorcontrib>Sahin, Nurhan</creatorcontrib><creatorcontrib>Sahin, Kazim</creatorcontrib><creatorcontrib>Koca, Suleyman Serdar</creatorcontrib><title>Epigallocatechin 3‐gallate attenuates arthritis by regulating Nrf2, HO‐1, and cytokine levels in an experimental arthritis model</title><title>Biotechnology and applied biochemistry</title><addtitle>BIOTECHNOL APPL BIOC</addtitle><addtitle>Biotechnol Appl Biochem</addtitle><description>Epigallocatechin 3‐gallate (EGCG) is a polyphenol that has been shown to have antioxidant and anti‐inflammatory effects. 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These results suggest that EGCG has an antiarthritic effect by regulating the oxidative‐antioxidant balance and cytokine levels in the CIA model, which is a surrogate experimental model of rheumatoid arthritis. EGCG applications, in experimental arthritis model, enhance the antioxidants enzyme levels and the expressions of Nrf‐2 and HO‐1. On the other hand, EGCG applications decrease the level of MDA, an oxidant, and the level of pro‐inflammatory cytokines. 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In this study, collagen‐induced arthritis (CIA) model, in Wistar albino rats, was used to elucidate the effect of EGCG on pathogenetic pathways in inflammatory arthritis. The levels of serum TNF‐α, IL‐17, malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx); the expression levels of tissue heme oxygenase‐1 (HO‐1) and nuclear factor erythroid 2‐related factor 2 (Nrf2); histopathologically, perisynovial inflammation and cartilage‐bone destruction were examined. In the sham group, serum TNF‐α, IL‐17, and MDA levels increased, while SOD, CAT, GPx levels, and the expressions of Nrf2 and HO‐1 decreased. On the other hand, in the EGCG administered groups, serum TNF‐α, IL‐17, and MDA levels improved, while SOD, CAT, GPx levels and the expressions of Nrf2 and HO‐1 increased. Moreover, histopathological analysis has shown that perisynovial inflammation and cartilage‐bone destruction decreased in the EGCG administered groups. These results suggest that EGCG has an antiarthritic effect by regulating the oxidative‐antioxidant balance and cytokine levels in the CIA model, which is a surrogate experimental model of rheumatoid arthritis. EGCG applications, in experimental arthritis model, enhance the antioxidants enzyme levels and the expressions of Nrf‐2 and HO‐1. On the other hand, EGCG applications decrease the level of MDA, an oxidant, and the level of pro‐inflammatory cytokines. Moreover, EGCG ameliorates the clinical and histological findings of inflammatory arthritis.</abstract><cop>HOBOKEN</cop><pub>Wiley</pub><pmid>31746064</pmid><doi>10.1002/bab.1860</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0003-4995-430X</orcidid><orcidid>https://orcid.org/0000-0002-6725-4182</orcidid><orcidid>https://orcid.org/0000-0003-4138-7689</orcidid><orcidid>https://orcid.org/0000-0003-4077-4134</orcidid><orcidid>https://orcid.org/0000-0001-9542-5244</orcidid></addata></record>
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subjects Animal models
Animals
Antioxidants
Arthritis
Arthritis, Experimental - chemically induced
Arthritis, Experimental - drug therapy
Arthritis, Experimental - metabolism
Biochemistry & Molecular Biology
Biotechnology & Applied Microbiology
Cartilage
Catalase
Catechin - analogs & derivatives
Catechin - pharmacology
Collagen
Collagen Type II
collagen‐induced arthritis
Cytokines
Cytokines - antagonists & inhibitors
Cytokines - biosynthesis
Destruction
Disease Models, Animal
Epigallocatechin-3-gallate
Female
Glutathione
Glutathione peroxidase
Heme
Heme Oxygenase (Decyclizing) - antagonists & inhibitors
Heme Oxygenase (Decyclizing) - biosynthesis
Inflammation
Life Sciences & Biomedicine
Malondialdehyde
NF-E2-Related Factor 2 - antagonists & inhibitors
NF-E2-Related Factor 2 - biosynthesis
Oxygenase
Peroxidase
Rats
Rats, Wistar
Rheumatoid arthritis
Science & Technology
Superoxide dismutase
Tumor necrosis factor
title Epigallocatechin 3‐gallate attenuates arthritis by regulating Nrf2, HO‐1, and cytokine levels in an experimental arthritis model
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