Decursin alleviates the aggravation of osteoarthritis via inhibiting PI3K-Akt and NF-kB signal pathway
•Decursin could improve the progression of osteoarthritis by inhibiting inflammatory reaction.•The molecular docking analysis showed that DE has a strong binding affinity with the inhibitory targets of PI3K.•Decursin may be a potential agent in treatment of osteoarthritis. Osteoarthritis (OA) is a c...
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description | •Decursin could improve the progression of osteoarthritis by inhibiting inflammatory reaction.•The molecular docking analysis showed that DE has a strong binding affinity with the inhibitory targets of PI3K.•Decursin may be a potential agent in treatment of osteoarthritis.
Osteoarthritis (OA) is a common joint disease that takes joint degeneration or aging as its pathological basis, and joint swelling, pain or dysfunction as its main clinical manifestations. Decursin (DE), the major active component isolated from Angelica gigas Nakai, has been demonstrated to possess anti-inflammatory effect in many diseases. But, the specific physiological mechanism of DE on OA is not clear yet. Therefore, the object of this study was to assess the therapeutic effect of DE on OA, and to explore its potential anti-inflammatory mechanisms. In vitro cell experiments, the inflammatory response in chondrocytes is mediated via interleukin-1β (IL-1β), which led to abnormal secretion of pro-inflammatory factors, such as prostaglandin E2 (PGE2), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), cyclooxygenase-2 (COX-2), nitric oxide (NO) and inducible nitric oxide synthase (iNOS). These cytokines were all decreased by the preconditioning of DE in a dose-dependent form of 1, 5, and 10 µM. Moreover, DE could restrain IL-1β-mediated inflammatory reaction and the collapse of extracellular matrix (ECM) via reducing the secretion of ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) and MMPs (matrix metalloproteinases). In short, DE restrained IL-1β-mediated abnormal excitation of PI3K/AKT/NF-κB axis. Furthermore, molecular docking analysis showed that DE has a strong binding affinity with the inhibitory targets of PI3K. In vivo animal studies, DE treatment could helped to improve destruction of articular cartilage and decreased the serum inflammatory factor levels in an operationally induced mouse OA model. To sum up, these data obtained from the experiment indicate that DE has good prospects for the treatment of osteoarthritis. |
doi_str_mv | 10.1016/j.intimp.2021.107657 |
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Osteoarthritis (OA) is a common joint disease that takes joint degeneration or aging as its pathological basis, and joint swelling, pain or dysfunction as its main clinical manifestations. Decursin (DE), the major active component isolated from Angelica gigas Nakai, has been demonstrated to possess anti-inflammatory effect in many diseases. But, the specific physiological mechanism of DE on OA is not clear yet. Therefore, the object of this study was to assess the therapeutic effect of DE on OA, and to explore its potential anti-inflammatory mechanisms. In vitro cell experiments, the inflammatory response in chondrocytes is mediated via interleukin-1β (IL-1β), which led to abnormal secretion of pro-inflammatory factors, such as prostaglandin E2 (PGE2), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), cyclooxygenase-2 (COX-2), nitric oxide (NO) and inducible nitric oxide synthase (iNOS). These cytokines were all decreased by the preconditioning of DE in a dose-dependent form of 1, 5, and 10 µM. Moreover, DE could restrain IL-1β-mediated inflammatory reaction and the collapse of extracellular matrix (ECM) via reducing the secretion of ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) and MMPs (matrix metalloproteinases). In short, DE restrained IL-1β-mediated abnormal excitation of PI3K/AKT/NF-κB axis. Furthermore, molecular docking analysis showed that DE has a strong binding affinity with the inhibitory targets of PI3K. In vivo animal studies, DE treatment could helped to improve destruction of articular cartilage and decreased the serum inflammatory factor levels in an operationally induced mouse OA model. To sum up, these data obtained from the experiment indicate that DE has good prospects for the treatment of osteoarthritis.</description><identifier>ISSN: 1567-5769</identifier><identifier>EISSN: 1878-1705</identifier><identifier>DOI: 10.1016/j.intimp.2021.107657</identifier><identifier>PMID: 33878544</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>1-Phosphatidylinositol 3-kinase ; ADAM protein ; Aging ; AKT protein ; Animals ; Anti-Inflammatory Agents - pharmacology ; Anti-Inflammatory Agents - therapeutic use ; Arthritis ; Benzopyrans - pharmacology ; Benzopyrans - therapeutic use ; Biomedical materials ; Butyrates - pharmacology ; Butyrates - therapeutic use ; Cartilage ; Cartilage (articular) ; Cartilage diseases ; Cartilage, Articular - drug effects ; Cartilage, Articular - immunology ; Cartilage, Articular - pathology ; Chondrocyte ; Chondrocytes ; Cyclooxygenase-2 ; Cytokines ; Decursin ; Degeneration ; Disease Progression ; Drug Evaluation, Preclinical ; Extracellular matrix ; Health services ; Humans ; IL-1β ; In vivo methods and tests ; Inflammatory ; Inflammatory response ; Interleukin 6 ; Interleukin-1beta - metabolism ; Joint diseases ; Male ; Matrix metalloproteinase ; Matrix metalloproteinases ; Mice ; Molecular docking ; Molecular Docking Simulation ; NF-kappa B - metabolism ; NF-κB ; NF-κB protein ; Nitric oxide ; Nitric-oxide synthase ; Osteoarthritis ; Osteoarthritis - drug therapy ; Osteoarthritis - immunology ; Osteoarthritis - pathology ; Pain ; Phosphatidylinositol 3-Kinases - metabolism ; Physiological effects ; PI3K ; Preconditioning ; Prostaglandin E2 ; Proto-Oncogene Proteins c-akt - metabolism ; Signal Transduction - drug effects ; Signal Transduction - immunology ; Thrombospondin ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>International immunopharmacology, 2021-08, Vol.97, p.107657-107657, Article 107657</ispartof><rights>2021 Elsevier B.V.</rights><rights>Copyright © 2021 Elsevier B.V. All rights reserved.</rights><rights>Copyright Elsevier BV Aug 2021</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-a57390429d6452855d49584da58022372a70b87f0965b3b246387a01b6ef63dd3</citedby><cites>FETCH-LOGICAL-c390t-a57390429d6452855d49584da58022372a70b87f0965b3b246387a01b6ef63dd3</cites><orcidid>0000-0003-0979-7207</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.intimp.2021.107657$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27926,27927,45997</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33878544$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>He, Linjie</creatorcontrib><creatorcontrib>Pan, Yinan</creatorcontrib><creatorcontrib>Yu, Jiapei</creatorcontrib><creatorcontrib>Wang, Ben</creatorcontrib><creatorcontrib>Dai, Gaole</creatorcontrib><creatorcontrib>Ying, Xiaozhou</creatorcontrib><title>Decursin alleviates the aggravation of osteoarthritis via inhibiting PI3K-Akt and NF-kB signal pathway</title><title>International immunopharmacology</title><addtitle>Int Immunopharmacol</addtitle><description>•Decursin could improve the progression of osteoarthritis by inhibiting inflammatory reaction.•The molecular docking analysis showed that DE has a strong binding affinity with the inhibitory targets of PI3K.•Decursin may be a potential agent in treatment of osteoarthritis.
Osteoarthritis (OA) is a common joint disease that takes joint degeneration or aging as its pathological basis, and joint swelling, pain or dysfunction as its main clinical manifestations. Decursin (DE), the major active component isolated from Angelica gigas Nakai, has been demonstrated to possess anti-inflammatory effect in many diseases. But, the specific physiological mechanism of DE on OA is not clear yet. Therefore, the object of this study was to assess the therapeutic effect of DE on OA, and to explore its potential anti-inflammatory mechanisms. In vitro cell experiments, the inflammatory response in chondrocytes is mediated via interleukin-1β (IL-1β), which led to abnormal secretion of pro-inflammatory factors, such as prostaglandin E2 (PGE2), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), cyclooxygenase-2 (COX-2), nitric oxide (NO) and inducible nitric oxide synthase (iNOS). These cytokines were all decreased by the preconditioning of DE in a dose-dependent form of 1, 5, and 10 µM. Moreover, DE could restrain IL-1β-mediated inflammatory reaction and the collapse of extracellular matrix (ECM) via reducing the secretion of ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) and MMPs (matrix metalloproteinases). In short, DE restrained IL-1β-mediated abnormal excitation of PI3K/AKT/NF-κB axis. Furthermore, molecular docking analysis showed that DE has a strong binding affinity with the inhibitory targets of PI3K. In vivo animal studies, DE treatment could helped to improve destruction of articular cartilage and decreased the serum inflammatory factor levels in an operationally induced mouse OA model. To sum up, these data obtained from the experiment indicate that DE has good prospects for the treatment of osteoarthritis.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>ADAM protein</subject><subject>Aging</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Arthritis</subject><subject>Benzopyrans - pharmacology</subject><subject>Benzopyrans - therapeutic use</subject><subject>Biomedical materials</subject><subject>Butyrates - pharmacology</subject><subject>Butyrates - therapeutic use</subject><subject>Cartilage</subject><subject>Cartilage (articular)</subject><subject>Cartilage diseases</subject><subject>Cartilage, Articular - drug effects</subject><subject>Cartilage, Articular - immunology</subject><subject>Cartilage, Articular - pathology</subject><subject>Chondrocyte</subject><subject>Chondrocytes</subject><subject>Cyclooxygenase-2</subject><subject>Cytokines</subject><subject>Decursin</subject><subject>Degeneration</subject><subject>Disease Progression</subject><subject>Drug Evaluation, Preclinical</subject><subject>Extracellular matrix</subject><subject>Health services</subject><subject>Humans</subject><subject>IL-1β</subject><subject>In vivo methods and tests</subject><subject>Inflammatory</subject><subject>Inflammatory response</subject><subject>Interleukin 6</subject><subject>Interleukin-1beta - metabolism</subject><subject>Joint diseases</subject><subject>Male</subject><subject>Matrix metalloproteinase</subject><subject>Matrix metalloproteinases</subject><subject>Mice</subject><subject>Molecular docking</subject><subject>Molecular Docking Simulation</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB</subject><subject>NF-κB protein</subject><subject>Nitric oxide</subject><subject>Nitric-oxide synthase</subject><subject>Osteoarthritis</subject><subject>Osteoarthritis - drug therapy</subject><subject>Osteoarthritis - immunology</subject><subject>Osteoarthritis - pathology</subject><subject>Pain</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Physiological effects</subject><subject>PI3K</subject><subject>Preconditioning</subject><subject>Prostaglandin E2</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - immunology</subject><subject>Thrombospondin</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><issn>1567-5769</issn><issn>1878-1705</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kctu1DAUhi0Eohd4A4QssWGTwXcnG6RSWqiogAWsLSc-mfE0Y09tZ1DfHo9SWLBgdS76zvVH6BUlK0qoerdd-VD8br9ihNGa0krqJ-iUtrptqCbyafWl0o3UqjtBZzlvCal5QZ-jE84rJYU4ReNHGOaUfcB2muDgbYGMywawXa-TPdjiY8BxxDEXiDaVTfLFZ1xB7MPG9zUKa_z9hn9pLu4KtsHhr9fN3Qec_TrYCe9t2fyyDy_Qs9FOGV4-2nP08_rqx-Xn5vbbp5vLi9tm4B0pjZW6WsE6p4RkrZROdLIVzsqWMMY1s5r0rR5Jp2TPeyZUPcQS2isYFXeOn6O3S999ivcz5GJ2Pg8wTTZAnLNhkirGNO3air75B93GOdWdj5RqCWdC80qJhRpSzDnBaPbJ72x6MJSYow5maxYdzFEHs-hQy14_Np_7Hbi_RX8eX4H3CwD1GwcPyeTBQxjA-QRDMS76_0_4DSrsmR8</recordid><startdate>202108</startdate><enddate>202108</enddate><creator>He, Linjie</creator><creator>Pan, Yinan</creator><creator>Yu, Jiapei</creator><creator>Wang, Ben</creator><creator>Dai, Gaole</creator><creator>Ying, Xiaozhou</creator><general>Elsevier B.V</general><general>Elsevier BV</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7T5</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-0979-7207</orcidid></search><sort><creationdate>202108</creationdate><title>Decursin alleviates the aggravation of osteoarthritis via inhibiting PI3K-Akt and NF-kB signal pathway</title><author>He, Linjie ; Pan, Yinan ; Yu, Jiapei ; Wang, Ben ; Dai, Gaole ; Ying, Xiaozhou</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-a57390429d6452855d49584da58022372a70b87f0965b3b246387a01b6ef63dd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>ADAM protein</topic><topic>Aging</topic><topic>AKT protein</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>Arthritis</topic><topic>Benzopyrans - pharmacology</topic><topic>Benzopyrans - therapeutic use</topic><topic>Biomedical materials</topic><topic>Butyrates - pharmacology</topic><topic>Butyrates - therapeutic use</topic><topic>Cartilage</topic><topic>Cartilage (articular)</topic><topic>Cartilage diseases</topic><topic>Cartilage, Articular - drug effects</topic><topic>Cartilage, Articular - immunology</topic><topic>Cartilage, Articular - pathology</topic><topic>Chondrocyte</topic><topic>Chondrocytes</topic><topic>Cyclooxygenase-2</topic><topic>Cytokines</topic><topic>Decursin</topic><topic>Degeneration</topic><topic>Disease Progression</topic><topic>Drug Evaluation, Preclinical</topic><topic>Extracellular matrix</topic><topic>Health services</topic><topic>Humans</topic><topic>IL-1β</topic><topic>In vivo methods and tests</topic><topic>Inflammatory</topic><topic>Inflammatory response</topic><topic>Interleukin 6</topic><topic>Interleukin-1beta - metabolism</topic><topic>Joint diseases</topic><topic>Male</topic><topic>Matrix metalloproteinase</topic><topic>Matrix metalloproteinases</topic><topic>Mice</topic><topic>Molecular docking</topic><topic>Molecular Docking Simulation</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB</topic><topic>NF-κB protein</topic><topic>Nitric oxide</topic><topic>Nitric-oxide synthase</topic><topic>Osteoarthritis</topic><topic>Osteoarthritis - drug therapy</topic><topic>Osteoarthritis - immunology</topic><topic>Osteoarthritis - pathology</topic><topic>Pain</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Physiological effects</topic><topic>PI3K</topic><topic>Preconditioning</topic><topic>Prostaglandin E2</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - immunology</topic><topic>Thrombospondin</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>He, Linjie</creatorcontrib><creatorcontrib>Pan, Yinan</creatorcontrib><creatorcontrib>Yu, Jiapei</creatorcontrib><creatorcontrib>Wang, Ben</creatorcontrib><creatorcontrib>Dai, Gaole</creatorcontrib><creatorcontrib>Ying, Xiaozhou</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International immunopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>He, Linjie</au><au>Pan, Yinan</au><au>Yu, Jiapei</au><au>Wang, Ben</au><au>Dai, Gaole</au><au>Ying, Xiaozhou</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Decursin alleviates the aggravation of osteoarthritis via inhibiting PI3K-Akt and NF-kB signal pathway</atitle><jtitle>International immunopharmacology</jtitle><addtitle>Int Immunopharmacol</addtitle><date>2021-08</date><risdate>2021</risdate><volume>97</volume><spage>107657</spage><epage>107657</epage><pages>107657-107657</pages><artnum>107657</artnum><issn>1567-5769</issn><eissn>1878-1705</eissn><abstract>•Decursin could improve the progression of osteoarthritis by inhibiting inflammatory reaction.•The molecular docking analysis showed that DE has a strong binding affinity with the inhibitory targets of PI3K.•Decursin may be a potential agent in treatment of osteoarthritis.
Osteoarthritis (OA) is a common joint disease that takes joint degeneration or aging as its pathological basis, and joint swelling, pain or dysfunction as its main clinical manifestations. Decursin (DE), the major active component isolated from Angelica gigas Nakai, has been demonstrated to possess anti-inflammatory effect in many diseases. But, the specific physiological mechanism of DE on OA is not clear yet. Therefore, the object of this study was to assess the therapeutic effect of DE on OA, and to explore its potential anti-inflammatory mechanisms. In vitro cell experiments, the inflammatory response in chondrocytes is mediated via interleukin-1β (IL-1β), which led to abnormal secretion of pro-inflammatory factors, such as prostaglandin E2 (PGE2), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), cyclooxygenase-2 (COX-2), nitric oxide (NO) and inducible nitric oxide synthase (iNOS). These cytokines were all decreased by the preconditioning of DE in a dose-dependent form of 1, 5, and 10 µM. Moreover, DE could restrain IL-1β-mediated inflammatory reaction and the collapse of extracellular matrix (ECM) via reducing the secretion of ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) and MMPs (matrix metalloproteinases). In short, DE restrained IL-1β-mediated abnormal excitation of PI3K/AKT/NF-κB axis. Furthermore, molecular docking analysis showed that DE has a strong binding affinity with the inhibitory targets of PI3K. In vivo animal studies, DE treatment could helped to improve destruction of articular cartilage and decreased the serum inflammatory factor levels in an operationally induced mouse OA model. To sum up, these data obtained from the experiment indicate that DE has good prospects for the treatment of osteoarthritis.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>33878544</pmid><doi>10.1016/j.intimp.2021.107657</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0003-0979-7207</orcidid></addata></record> |
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subjects | 1-Phosphatidylinositol 3-kinase ADAM protein Aging AKT protein Animals Anti-Inflammatory Agents - pharmacology Anti-Inflammatory Agents - therapeutic use Arthritis Benzopyrans - pharmacology Benzopyrans - therapeutic use Biomedical materials Butyrates - pharmacology Butyrates - therapeutic use Cartilage Cartilage (articular) Cartilage diseases Cartilage, Articular - drug effects Cartilage, Articular - immunology Cartilage, Articular - pathology Chondrocyte Chondrocytes Cyclooxygenase-2 Cytokines Decursin Degeneration Disease Progression Drug Evaluation, Preclinical Extracellular matrix Health services Humans IL-1β In vivo methods and tests Inflammatory Inflammatory response Interleukin 6 Interleukin-1beta - metabolism Joint diseases Male Matrix metalloproteinase Matrix metalloproteinases Mice Molecular docking Molecular Docking Simulation NF-kappa B - metabolism NF-κB NF-κB protein Nitric oxide Nitric-oxide synthase Osteoarthritis Osteoarthritis - drug therapy Osteoarthritis - immunology Osteoarthritis - pathology Pain Phosphatidylinositol 3-Kinases - metabolism Physiological effects PI3K Preconditioning Prostaglandin E2 Proto-Oncogene Proteins c-akt - metabolism Signal Transduction - drug effects Signal Transduction - immunology Thrombospondin Tumor necrosis factor-TNF Tumor necrosis factor-α |
title | Decursin alleviates the aggravation of osteoarthritis via inhibiting PI3K-Akt and NF-kB signal pathway |
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