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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Veröffentlicht in:Oxidative medicine and cellular longevity 2021, Vol.2021 (1), p.8684725-8684725
Hauptverfasser: 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
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container_issue 1
container_start_page 8684725
container_title Oxidative medicine and cellular longevity
container_volume 2021
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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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 &amp; 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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. 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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
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