BST204 Protects Dexamethasone-Induced Myotube Atrophy through the Upregulation of Myotube Formation and Mitochondrial Function
BST204 is a purified ginseng dry extract that has an inhibitory effect on lipopolysaccharide-induced inflammatory responses, but its effect on muscle atrophy is yet to be investigated. In this study, C2C12 myoblasts were induced to differentiate for three days followed by the treatment of dexamethas...
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description | BST204 is a purified ginseng dry extract that has an inhibitory effect on lipopolysaccharide-induced inflammatory responses, but its effect on muscle atrophy is yet to be investigated. In this study, C2C12 myoblasts were induced to differentiate for three days followed by the treatment of dexamethasone (DEX), a corticosteroid drug, with vehicle or BST204 for one day and subjected to immunoblotting, immunocytochemistry, qRT-PCR and biochemical analysis for mitochondrial function. BST204 alleviates the myotube atrophic effect mediated by DEX via the activation of protein kinase B/mammalian target of rapamycin (Akt/mTOR) signaling. Through this pathway, BST204 suppresses the expression of muscle-specific E3 ubiquitin ligases contributing to the enhanced myotube formation and enlarged myotube diameter in DEX-treated myotubes. In addition, BST204 treatment significantly decreases the mitochondrial reactive oxygen species production in DEX-treated myotubes. Furthermore, BST204 improves mitochondrial function by upregulating the expression of peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC1 alpha) in DEX-induced myotube atrophy. This study provides a mechanistic insight into the effect of BST204 on DEX-induced myotube atrophy, suggesting that BST204 has protective effects against the toxicity of a corticosteroid drug in muscle and promising potential as a nutraceutical remedy for the treatment of muscle weakness and atrophy. |
doi_str_mv | 10.3390/ijerph18052367 |
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In this study, C2C12 myoblasts were induced to differentiate for three days followed by the treatment of dexamethasone (DEX), a corticosteroid drug, with vehicle or BST204 for one day and subjected to immunoblotting, immunocytochemistry, qRT-PCR and biochemical analysis for mitochondrial function. BST204 alleviates the myotube atrophic effect mediated by DEX via the activation of protein kinase B/mammalian target of rapamycin (Akt/mTOR) signaling. Through this pathway, BST204 suppresses the expression of muscle-specific E3 ubiquitin ligases contributing to the enhanced myotube formation and enlarged myotube diameter in DEX-treated myotubes. In addition, BST204 treatment significantly decreases the mitochondrial reactive oxygen species production in DEX-treated myotubes. Furthermore, BST204 improves mitochondrial function by upregulating the expression of peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC1 alpha) in DEX-induced myotube atrophy. This study provides a mechanistic insight into the effect of BST204 on DEX-induced myotube atrophy, suggesting that BST204 has protective effects against the toxicity of a corticosteroid drug in muscle and promising potential as a nutraceutical remedy for the treatment of muscle weakness and atrophy.</description><identifier>ISSN: 1660-4601</identifier><identifier>ISSN: 1661-7827</identifier><identifier>EISSN: 1660-4601</identifier><identifier>DOI: 10.3390/ijerph18052367</identifier><identifier>PMID: 33804338</identifier><language>eng</language><publisher>BASEL: Mdpi</publisher><subject>Dexamethasone - toxicity ; Environmental Sciences ; Environmental Sciences & Ecology ; Humans ; Life Sciences & Biomedicine ; Mitochondria ; Muscle Fibers, Skeletal - metabolism ; Muscle, Skeletal ; Muscular Atrophy - chemically induced ; Muscular Atrophy - drug therapy ; Muscular Atrophy - prevention & control ; Public, Environmental & Occupational Health ; Science & Technology ; Up-Regulation</subject><ispartof>International journal of environmental research and public health, 2021-03, Vol.18 (5), p.2367, Article 2367</ispartof><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>7</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000628153800001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c390t-b176270e2604fb62147f39876072c3f15031e50bf0eedd736d6e9ef5d5143acf3</citedby><cites>FETCH-LOGICAL-c390t-b176270e2604fb62147f39876072c3f15031e50bf0eedd736d6e9ef5d5143acf3</cites><orcidid>0000-0002-4386-6934</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/PMC7957540/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7957540/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,27929,27930,39262,39263,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33804338$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Ryuni</creatorcontrib><creatorcontrib>Kim, Hyebeen</creatorcontrib><creatorcontrib>Im, Minju</creatorcontrib><creatorcontrib>Park, Sun Kyu</creatorcontrib><creatorcontrib>Han, Hae Jung</creatorcontrib><creatorcontrib>An, Subin</creatorcontrib><creatorcontrib>Kang, Jong-Sun</creatorcontrib><creatorcontrib>Lee, Sang-Jin</creatorcontrib><creatorcontrib>Bae, Gyu-Un</creatorcontrib><title>BST204 Protects Dexamethasone-Induced Myotube Atrophy through the Upregulation of Myotube Formation and Mitochondrial Function</title><title>International journal of environmental research and public health</title><addtitle>INT J ENV RES PUB HE</addtitle><addtitle>Int J Environ Res Public Health</addtitle><description>BST204 is a purified ginseng dry extract that has an inhibitory effect on lipopolysaccharide-induced inflammatory responses, but its effect on muscle atrophy is yet to be investigated. In this study, C2C12 myoblasts were induced to differentiate for three days followed by the treatment of dexamethasone (DEX), a corticosteroid drug, with vehicle or BST204 for one day and subjected to immunoblotting, immunocytochemistry, qRT-PCR and biochemical analysis for mitochondrial function. BST204 alleviates the myotube atrophic effect mediated by DEX via the activation of protein kinase B/mammalian target of rapamycin (Akt/mTOR) signaling. Through this pathway, BST204 suppresses the expression of muscle-specific E3 ubiquitin ligases contributing to the enhanced myotube formation and enlarged myotube diameter in DEX-treated myotubes. In addition, BST204 treatment significantly decreases the mitochondrial reactive oxygen species production in DEX-treated myotubes. Furthermore, BST204 improves mitochondrial function by upregulating the expression of peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC1 alpha) in DEX-induced myotube atrophy. This study provides a mechanistic insight into the effect of BST204 on DEX-induced myotube atrophy, suggesting that BST204 has protective effects against the toxicity of a corticosteroid drug in muscle and promising potential as a nutraceutical remedy for the treatment of muscle weakness and atrophy.</description><subject>Dexamethasone - toxicity</subject><subject>Environmental Sciences</subject><subject>Environmental Sciences & Ecology</subject><subject>Humans</subject><subject>Life Sciences & Biomedicine</subject><subject>Mitochondria</subject><subject>Muscle Fibers, Skeletal - metabolism</subject><subject>Muscle, Skeletal</subject><subject>Muscular Atrophy - chemically induced</subject><subject>Muscular Atrophy - drug therapy</subject><subject>Muscular Atrophy - prevention & control</subject><subject>Public, Environmental & Occupational Health</subject><subject>Science & Technology</subject><subject>Up-Regulation</subject><issn>1660-4601</issn><issn>1661-7827</issn><issn>1660-4601</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>GIZIO</sourceid><sourceid>HGBXW</sourceid><sourceid>EIF</sourceid><recordid>eNqNkdFP2zAQxq2JaRTY6x5R3lG6c5zYyQtS6eiGxLRJwHPkOOfGVWtHjgPrC387Zt0q-oYffNbd7_usuyPkC4UpYxV8NSv0fUdLKDLGxQcyoZxDmnOgR2_ex-RkGFYArMx59YkcM1ZCHq8Jeb66u88gT357F1CFIfmGf-QGQycHZzG9se2osE1-bl0YG0xmwbu-2yah825cdjFi8tB7XI5rGYyzidN7duH8ZpeUNjqY4FTnbOuNXCeL0arX0hn5qOV6wM__4il5WFzfz3-kt7--38xnt6mKTYa0oYJnAjDjkOuGZzQXmlWl4CAyxTQtgFEsoNGA2LaC8ZZjhbpoC5ozqTQ7JZc7335sNtgqtMHLdd17s5F-Wztp6sOKNV29dI-1qApR5BANpjsD5d0weNR7LYX6dRP14Sai4Pztj3v8_-gjUO6AJ2ycHpRBq3CPAQDPSlpEOh46N-HvKOdutCFKL94vZS-aeKmR</recordid><startdate>20210301</startdate><enddate>20210301</enddate><creator>Kim, Ryuni</creator><creator>Kim, Hyebeen</creator><creator>Im, Minju</creator><creator>Park, Sun Kyu</creator><creator>Han, Hae Jung</creator><creator>An, Subin</creator><creator>Kang, Jong-Sun</creator><creator>Lee, Sang-Jin</creator><creator>Bae, Gyu-Un</creator><general>Mdpi</general><general>MDPI</general><scope>17B</scope><scope>BLEPL</scope><scope>DTL</scope><scope>DVR</scope><scope>EGQ</scope><scope>GIZIO</scope><scope>HGBXW</scope><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>5PM</scope><orcidid>https://orcid.org/0000-0002-4386-6934</orcidid></search><sort><creationdate>20210301</creationdate><title>BST204 Protects Dexamethasone-Induced Myotube Atrophy through the Upregulation of Myotube Formation and Mitochondrial Function</title><author>Kim, Ryuni ; Kim, Hyebeen ; Im, Minju ; Park, Sun Kyu ; Han, Hae Jung ; An, Subin ; Kang, Jong-Sun ; Lee, Sang-Jin ; Bae, Gyu-Un</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-b176270e2604fb62147f39876072c3f15031e50bf0eedd736d6e9ef5d5143acf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Dexamethasone - toxicity</topic><topic>Environmental Sciences</topic><topic>Environmental Sciences & Ecology</topic><topic>Humans</topic><topic>Life Sciences & Biomedicine</topic><topic>Mitochondria</topic><topic>Muscle Fibers, Skeletal - metabolism</topic><topic>Muscle, Skeletal</topic><topic>Muscular Atrophy - chemically induced</topic><topic>Muscular Atrophy - drug therapy</topic><topic>Muscular Atrophy - prevention & control</topic><topic>Public, Environmental & Occupational Health</topic><topic>Science & Technology</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Ryuni</creatorcontrib><creatorcontrib>Kim, Hyebeen</creatorcontrib><creatorcontrib>Im, Minju</creatorcontrib><creatorcontrib>Park, Sun Kyu</creatorcontrib><creatorcontrib>Han, Hae Jung</creatorcontrib><creatorcontrib>An, Subin</creatorcontrib><creatorcontrib>Kang, Jong-Sun</creatorcontrib><creatorcontrib>Lee, Sang-Jin</creatorcontrib><creatorcontrib>Bae, Gyu-Un</creatorcontrib><collection>Web of Knowledge</collection><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Social Sciences Citation Index</collection><collection>Web of Science Primary (SCIE, SSCI & AHCI)</collection><collection>Web of Science - Social Sciences Citation Index – 2021</collection><collection>Web of Science - Science Citation Index Expanded - 2021</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of environmental research and public health</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Ryuni</au><au>Kim, Hyebeen</au><au>Im, Minju</au><au>Park, Sun Kyu</au><au>Han, Hae Jung</au><au>An, Subin</au><au>Kang, Jong-Sun</au><au>Lee, Sang-Jin</au><au>Bae, Gyu-Un</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>BST204 Protects Dexamethasone-Induced Myotube Atrophy through the Upregulation of Myotube Formation and Mitochondrial Function</atitle><jtitle>International journal of environmental research and public health</jtitle><stitle>INT J ENV RES PUB HE</stitle><addtitle>Int J Environ Res Public Health</addtitle><date>2021-03-01</date><risdate>2021</risdate><volume>18</volume><issue>5</issue><spage>2367</spage><pages>2367-</pages><artnum>2367</artnum><issn>1660-4601</issn><issn>1661-7827</issn><eissn>1660-4601</eissn><abstract>BST204 is a purified ginseng dry extract that has an inhibitory effect on lipopolysaccharide-induced inflammatory responses, but its effect on muscle atrophy is yet to be investigated. In this study, C2C12 myoblasts were induced to differentiate for three days followed by the treatment of dexamethasone (DEX), a corticosteroid drug, with vehicle or BST204 for one day and subjected to immunoblotting, immunocytochemistry, qRT-PCR and biochemical analysis for mitochondrial function. BST204 alleviates the myotube atrophic effect mediated by DEX via the activation of protein kinase B/mammalian target of rapamycin (Akt/mTOR) signaling. Through this pathway, BST204 suppresses the expression of muscle-specific E3 ubiquitin ligases contributing to the enhanced myotube formation and enlarged myotube diameter in DEX-treated myotubes. In addition, BST204 treatment significantly decreases the mitochondrial reactive oxygen species production in DEX-treated myotubes. Furthermore, BST204 improves mitochondrial function by upregulating the expression of peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC1 alpha) in DEX-induced myotube atrophy. This study provides a mechanistic insight into the effect of BST204 on DEX-induced myotube atrophy, suggesting that BST204 has protective effects against the toxicity of a corticosteroid drug in muscle and promising potential as a nutraceutical remedy for the treatment of muscle weakness and atrophy.</abstract><cop>BASEL</cop><pub>Mdpi</pub><pmid>33804338</pmid><doi>10.3390/ijerph18052367</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-4386-6934</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Dexamethasone - toxicity Environmental Sciences Environmental Sciences & Ecology Humans Life Sciences & Biomedicine Mitochondria Muscle Fibers, Skeletal - metabolism Muscle, Skeletal Muscular Atrophy - chemically induced Muscular Atrophy - drug therapy Muscular Atrophy - prevention & control Public, Environmental & Occupational Health Science & Technology Up-Regulation |
title | BST204 Protects Dexamethasone-Induced Myotube Atrophy through the Upregulation of Myotube Formation and Mitochondrial Function |
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