Acteoside Counteracts Interleukin-1β-Induced Catabolic Processes through the Modulation of Mitogen-Activated Protein Kinases and the NFκB Cellular Signaling Pathway
Osteoarthritis (OA) is the most common degenerative joint disease with chronic joint pain caused by progressive degeneration of articular cartilage at synovial joints. Acteoside, a caffeoylphenylethanoid glycoside, has various biological activities such as antimicrobial, anti-inflammatory, anticance...
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creator | Lim, HyangI Kim, Do Kyung Kim, Tae-Hyeon Kang, Kyeong-Rok Seo, Jeong-Yeon Cho, Seung Sik Yun, Younghee Choi, Ye-yong Leem, Jungtae Kim, Hyoun-Woo Jo, Geon-Ung Oh, Chan-Jin Oh, Deuk-Sil Chun, Hong-Sung Kim, Jae-Sung |
description | Osteoarthritis (OA) is the most common degenerative joint disease with chronic joint pain caused by progressive degeneration of articular cartilage at synovial joints. Acteoside, a caffeoylphenylethanoid glycoside, has various biological activities such as antimicrobial, anti-inflammatory, anticancer, antioxidative, cytoprotective, and neuroprotective effect. Further, oral administration of acteoside at high dosage does not cause genotoxicity. Therefore, the aim of present study is to verify the anticatabolic effects of acteoside against osteoarthritis and its anticatabolic signaling pathway. Acteoside did not decrease the viabilities of mouse fibroblast L929 cells used as normal cells and primary rat chondrocytes. Acteoside counteracted the IL-1β-induced proteoglycan loss in the chondrocytes and articular cartilage through suppressing the expression and activation of cartilage-degrading enzyme such as matrix metalloproteinase- (MMP-) 13, MMP-1, and MMP-3. Furthermore, acteoside suppressed the expression of inflammatory mediators such as inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, and prostaglandin E2 in the primary rat chondrocytes treated with IL-1β. Subsequently, the expression of proinflammatory cytokines was decreased by acteoside in the primary rat chondrocytes treated with IL-1β. Moreover, acteoside suppressed not only the phosphorylation of mitogen-activated protein kinases in primary rat chondrocytes treated with IL-1β but also the translocation of NFκB from the cytosol to the nucleus through suppression of its phosphorylation. Oral administration of 5 and 10 mg/kg acteoside attenuated the progressive degeneration of articular cartilage in the osteoarthritic mouse model generated by destabilization of the medial meniscus. Our findings indicate that acteoside is a promising potential anticatabolic agent or supplement to attenuate or prevent progressive degeneration of articular cartilage. |
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Acteoside, a caffeoylphenylethanoid glycoside, has various biological activities such as antimicrobial, anti-inflammatory, anticancer, antioxidative, cytoprotective, and neuroprotective effect. Further, oral administration of acteoside at high dosage does not cause genotoxicity. Therefore, the aim of present study is to verify the anticatabolic effects of acteoside against osteoarthritis and its anticatabolic signaling pathway. Acteoside did not decrease the viabilities of mouse fibroblast L929 cells used as normal cells and primary rat chondrocytes. Acteoside counteracted the IL-1β-induced proteoglycan loss in the chondrocytes and articular cartilage through suppressing the expression and activation of cartilage-degrading enzyme such as matrix metalloproteinase- (MMP-) 13, MMP-1, and MMP-3. Furthermore, acteoside suppressed the expression of inflammatory mediators such as inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, and prostaglandin E2 in the primary rat chondrocytes treated with IL-1β. Subsequently, the expression of proinflammatory cytokines was decreased by acteoside in the primary rat chondrocytes treated with IL-1β. Moreover, acteoside suppressed not only the phosphorylation of mitogen-activated protein kinases in primary rat chondrocytes treated with IL-1β but also the translocation of NFκB from the cytosol to the nucleus through suppression of its phosphorylation. Oral administration of 5 and 10 mg/kg acteoside attenuated the progressive degeneration of articular cartilage in the osteoarthritic mouse model generated by destabilization of the medial meniscus. Our findings indicate that acteoside is a promising potential anticatabolic agent or supplement to attenuate or prevent progressive degeneration of articular cartilage.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2021/8684725</identifier><identifier>PMID: 33833854</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>Acids ; Cartilage ; Enzymes ; Fibroblasts ; Kinases ; Older people ; Pain ; Penicillin ; Proteins</subject><ispartof>Oxidative medicine and cellular longevity, 2021, Vol.2021 (1), p.8684725-8684725</ispartof><rights>Copyright © 2021 HyangI Lim et al.</rights><rights>Copyright © 2021 HyangI Lim et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2021 HyangI Lim et al. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-8e2b22c0982d5f4a493f62a05d04cf930ba3e525316b14446c441d990e3cab423</citedby><cites>FETCH-LOGICAL-c448t-8e2b22c0982d5f4a493f62a05d04cf930ba3e525316b14446c441d990e3cab423</cites><orcidid>0000-0002-9290-364X ; 0000-0003-1497-0529 ; 0000-0001-6254-946X ; 0000-0003-1369-3865 ; 0000-0002-9835-6632 ; 0000-0002-3584-6351 ; 0000-0002-6724-3459 ; 0000-0001-8489-8476 ; 0000-0002-2544-8608 ; 0000-0003-3300-5556 ; 0000-0001-8621-5325 ; 0000-0001-7582-6761 ; 0000-0002-2728-4205 ; 0000-0002-8592-6405 ; 0000-0003-4174-0139</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8016581/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8016581/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4022,27922,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33833854$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Drevet, Joël R.</contributor><contributor>Joël R Drevet</contributor><creatorcontrib>Lim, HyangI</creatorcontrib><creatorcontrib>Kim, Do Kyung</creatorcontrib><creatorcontrib>Kim, Tae-Hyeon</creatorcontrib><creatorcontrib>Kang, Kyeong-Rok</creatorcontrib><creatorcontrib>Seo, Jeong-Yeon</creatorcontrib><creatorcontrib>Cho, Seung Sik</creatorcontrib><creatorcontrib>Yun, Younghee</creatorcontrib><creatorcontrib>Choi, Ye-yong</creatorcontrib><creatorcontrib>Leem, Jungtae</creatorcontrib><creatorcontrib>Kim, Hyoun-Woo</creatorcontrib><creatorcontrib>Jo, Geon-Ung</creatorcontrib><creatorcontrib>Oh, Chan-Jin</creatorcontrib><creatorcontrib>Oh, Deuk-Sil</creatorcontrib><creatorcontrib>Chun, Hong-Sung</creatorcontrib><creatorcontrib>Kim, Jae-Sung</creatorcontrib><title>Acteoside Counteracts Interleukin-1β-Induced Catabolic Processes through the Modulation of Mitogen-Activated Protein Kinases and the NFκB Cellular Signaling Pathway</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Osteoarthritis (OA) is the most common degenerative joint disease with chronic joint pain caused by progressive degeneration of articular cartilage at synovial joints. Acteoside, a caffeoylphenylethanoid glycoside, has various biological activities such as antimicrobial, anti-inflammatory, anticancer, antioxidative, cytoprotective, and neuroprotective effect. Further, oral administration of acteoside at high dosage does not cause genotoxicity. Therefore, the aim of present study is to verify the anticatabolic effects of acteoside against osteoarthritis and its anticatabolic signaling pathway. Acteoside did not decrease the viabilities of mouse fibroblast L929 cells used as normal cells and primary rat chondrocytes. Acteoside counteracted the IL-1β-induced proteoglycan loss in the chondrocytes and articular cartilage through suppressing the expression and activation of cartilage-degrading enzyme such as matrix metalloproteinase- (MMP-) 13, MMP-1, and MMP-3. Furthermore, acteoside suppressed the expression of inflammatory mediators such as inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, and prostaglandin E2 in the primary rat chondrocytes treated with IL-1β. Subsequently, the expression of proinflammatory cytokines was decreased by acteoside in the primary rat chondrocytes treated with IL-1β. Moreover, acteoside suppressed not only the phosphorylation of mitogen-activated protein kinases in primary rat chondrocytes treated with IL-1β but also the translocation of NFκB from the cytosol to the nucleus through suppression of its phosphorylation. Oral administration of 5 and 10 mg/kg acteoside attenuated the progressive degeneration of articular cartilage in the osteoarthritic mouse model generated by destabilization of the medial meniscus. Our findings indicate that acteoside is a promising potential anticatabolic agent or supplement to attenuate or prevent progressive degeneration of articular cartilage.</description><subject>Acids</subject><subject>Cartilage</subject><subject>Enzymes</subject><subject>Fibroblasts</subject><subject>Kinases</subject><subject>Older people</subject><subject>Pain</subject><subject>Penicillin</subject><subject>Proteins</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9ks9qFTEUxgdRbK3uXEvAjaBj83ec2Qh1sHqx1YK6DpnkzEzq3KQmmZa-kA_g0ofoM5nxXi_qQgicA_l938khX1E8JPg5IUIcUkzJYV3V_AUVt4p90nBa4qbht3c9xnvFvRjPMa4Y5eRuscdYnY_g-8W3I53AR2sAtX52CYLSKaLV0k0wf7GuJDffy5UzswaDWpVU5yer0VnwGmKEiNIY_DyMuQI69WaeVLLeId-jU5v8AK7MM-ylSlmfVQmsQ--sU4tWOfNL9_745scr1MI0ZXlAH-3g1GTdgM5UGq_U9f3iTq-mCA-29aD4fPz6U_u2PPnwZtUenZSa8zqVNdCOUo2bmhrRc8Ub1ldUYWEw133DcKcYCCoYqTrCOa-yjJimwcC06jhlB8XLje_F3K3BaHApqEleBLtW4Vp6ZeXfN86OcvCXssakEjXJBk-2BsF_nSEmubZR572UAz9HSQUhlFeMs4w-_gc993PIey8Urmn2a3Cmnm0oHXyMAfrdYwiWSwDkEgC5DUDGH_25wA7-_eMZeLoBRuuMurL_t_sJyDq8EQ</recordid><startdate>2021</startdate><enddate>2021</enddate><creator>Lim, HyangI</creator><creator>Kim, Do Kyung</creator><creator>Kim, Tae-Hyeon</creator><creator>Kang, Kyeong-Rok</creator><creator>Seo, Jeong-Yeon</creator><creator>Cho, Seung Sik</creator><creator>Yun, Younghee</creator><creator>Choi, Ye-yong</creator><creator>Leem, Jungtae</creator><creator>Kim, Hyoun-Woo</creator><creator>Jo, Geon-Ung</creator><creator>Oh, Chan-Jin</creator><creator>Oh, Deuk-Sil</creator><creator>Chun, Hong-Sung</creator><creator>Kim, Jae-Sung</creator><general>Hindawi</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-9290-364X</orcidid><orcidid>https://orcid.org/0000-0003-1497-0529</orcidid><orcidid>https://orcid.org/0000-0001-6254-946X</orcidid><orcidid>https://orcid.org/0000-0003-1369-3865</orcidid><orcidid>https://orcid.org/0000-0002-9835-6632</orcidid><orcidid>https://orcid.org/0000-0002-3584-6351</orcidid><orcidid>https://orcid.org/0000-0002-6724-3459</orcidid><orcidid>https://orcid.org/0000-0001-8489-8476</orcidid><orcidid>https://orcid.org/0000-0002-2544-8608</orcidid><orcidid>https://orcid.org/0000-0003-3300-5556</orcidid><orcidid>https://orcid.org/0000-0001-8621-5325</orcidid><orcidid>https://orcid.org/0000-0001-7582-6761</orcidid><orcidid>https://orcid.org/0000-0002-2728-4205</orcidid><orcidid>https://orcid.org/0000-0002-8592-6405</orcidid><orcidid>https://orcid.org/0000-0003-4174-0139</orcidid></search><sort><creationdate>2021</creationdate><title>Acteoside Counteracts Interleukin-1β-Induced Catabolic Processes through the Modulation of Mitogen-Activated Protein Kinases and the NFκB Cellular Signaling Pathway</title><author>Lim, HyangI ; Kim, Do Kyung ; Kim, Tae-Hyeon ; Kang, Kyeong-Rok ; Seo, Jeong-Yeon ; Cho, Seung Sik ; Yun, Younghee ; Choi, Ye-yong ; Leem, Jungtae ; Kim, Hyoun-Woo ; Jo, Geon-Ung ; Oh, Chan-Jin ; Oh, Deuk-Sil ; Chun, Hong-Sung ; Kim, Jae-Sung</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-8e2b22c0982d5f4a493f62a05d04cf930ba3e525316b14446c441d990e3cab423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Acids</topic><topic>Cartilage</topic><topic>Enzymes</topic><topic>Fibroblasts</topic><topic>Kinases</topic><topic>Older people</topic><topic>Pain</topic><topic>Penicillin</topic><topic>Proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lim, HyangI</creatorcontrib><creatorcontrib>Kim, Do Kyung</creatorcontrib><creatorcontrib>Kim, Tae-Hyeon</creatorcontrib><creatorcontrib>Kang, Kyeong-Rok</creatorcontrib><creatorcontrib>Seo, Jeong-Yeon</creatorcontrib><creatorcontrib>Cho, Seung Sik</creatorcontrib><creatorcontrib>Yun, Younghee</creatorcontrib><creatorcontrib>Choi, Ye-yong</creatorcontrib><creatorcontrib>Leem, Jungtae</creatorcontrib><creatorcontrib>Kim, Hyoun-Woo</creatorcontrib><creatorcontrib>Jo, Geon-Ung</creatorcontrib><creatorcontrib>Oh, Chan-Jin</creatorcontrib><creatorcontrib>Oh, Deuk-Sil</creatorcontrib><creatorcontrib>Chun, Hong-Sung</creatorcontrib><creatorcontrib>Kim, Jae-Sung</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lim, HyangI</au><au>Kim, Do Kyung</au><au>Kim, Tae-Hyeon</au><au>Kang, Kyeong-Rok</au><au>Seo, Jeong-Yeon</au><au>Cho, Seung Sik</au><au>Yun, Younghee</au><au>Choi, Ye-yong</au><au>Leem, Jungtae</au><au>Kim, Hyoun-Woo</au><au>Jo, Geon-Ung</au><au>Oh, Chan-Jin</au><au>Oh, Deuk-Sil</au><au>Chun, Hong-Sung</au><au>Kim, Jae-Sung</au><au>Drevet, Joël R.</au><au>Joël R Drevet</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acteoside Counteracts Interleukin-1β-Induced Catabolic Processes through the Modulation of Mitogen-Activated Protein Kinases and the NFκB Cellular Signaling Pathway</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2021</date><risdate>2021</risdate><volume>2021</volume><issue>1</issue><spage>8684725</spage><epage>8684725</epage><pages>8684725-8684725</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Osteoarthritis (OA) is the most common degenerative joint disease with chronic joint pain caused by progressive degeneration of articular cartilage at synovial joints. Acteoside, a caffeoylphenylethanoid glycoside, has various biological activities such as antimicrobial, anti-inflammatory, anticancer, antioxidative, cytoprotective, and neuroprotective effect. Further, oral administration of acteoside at high dosage does not cause genotoxicity. Therefore, the aim of present study is to verify the anticatabolic effects of acteoside against osteoarthritis and its anticatabolic signaling pathway. Acteoside did not decrease the viabilities of mouse fibroblast L929 cells used as normal cells and primary rat chondrocytes. Acteoside counteracted the IL-1β-induced proteoglycan loss in the chondrocytes and articular cartilage through suppressing the expression and activation of cartilage-degrading enzyme such as matrix metalloproteinase- (MMP-) 13, MMP-1, and MMP-3. Furthermore, acteoside suppressed the expression of inflammatory mediators such as inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, and prostaglandin E2 in the primary rat chondrocytes treated with IL-1β. Subsequently, the expression of proinflammatory cytokines was decreased by acteoside in the primary rat chondrocytes treated with IL-1β. Moreover, acteoside suppressed not only the phosphorylation of mitogen-activated protein kinases in primary rat chondrocytes treated with IL-1β but also the translocation of NFκB from the cytosol to the nucleus through suppression of its phosphorylation. Oral administration of 5 and 10 mg/kg acteoside attenuated the progressive degeneration of articular cartilage in the osteoarthritic mouse model generated by destabilization of the medial meniscus. Our findings indicate that acteoside is a promising potential anticatabolic agent or supplement to attenuate or prevent progressive degeneration of articular cartilage.</abstract><cop>United States</cop><pub>Hindawi</pub><pmid>33833854</pmid><doi>10.1155/2021/8684725</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-9290-364X</orcidid><orcidid>https://orcid.org/0000-0003-1497-0529</orcidid><orcidid>https://orcid.org/0000-0001-6254-946X</orcidid><orcidid>https://orcid.org/0000-0003-1369-3865</orcidid><orcidid>https://orcid.org/0000-0002-9835-6632</orcidid><orcidid>https://orcid.org/0000-0002-3584-6351</orcidid><orcidid>https://orcid.org/0000-0002-6724-3459</orcidid><orcidid>https://orcid.org/0000-0001-8489-8476</orcidid><orcidid>https://orcid.org/0000-0002-2544-8608</orcidid><orcidid>https://orcid.org/0000-0003-3300-5556</orcidid><orcidid>https://orcid.org/0000-0001-8621-5325</orcidid><orcidid>https://orcid.org/0000-0001-7582-6761</orcidid><orcidid>https://orcid.org/0000-0002-2728-4205</orcidid><orcidid>https://orcid.org/0000-0002-8592-6405</orcidid><orcidid>https://orcid.org/0000-0003-4174-0139</orcidid><oa>free_for_read</oa></addata></record> |
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source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; Wiley-Blackwell Open Access Titles; PubMed Central; Alma/SFX Local Collection |
subjects | Acids Cartilage Enzymes Fibroblasts Kinases Older people Pain Penicillin Proteins |
title | Acteoside Counteracts Interleukin-1β-Induced Catabolic Processes through the Modulation of Mitogen-Activated Protein Kinases and the NFκB Cellular Signaling Pathway |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-11T08%3A19%3A44IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Acteoside%20Counteracts%20Interleukin-1%CE%B2-Induced%20Catabolic%20Processes%20through%20the%20Modulation%20of%20Mitogen-Activated%20Protein%20Kinases%20and%20the%20NF%CE%BAB%20Cellular%20Signaling%20Pathway&rft.jtitle=Oxidative%20medicine%20and%20cellular%20longevity&rft.au=Lim,%20HyangI&rft.date=2021&rft.volume=2021&rft.issue=1&rft.spage=8684725&rft.epage=8684725&rft.pages=8684725-8684725&rft.issn=1942-0900&rft.eissn=1942-0994&rft_id=info:doi/10.1155/2021/8684725&rft_dat=%3Cproquest_pubme%3E2508265890%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2508265890&rft_id=info:pmid/33833854&rfr_iscdi=true |