Baicalin Suppresses the Proliferation and Migration of Ox-LDL-VSMCs in Atherosclerosis through Upregulating miR-126-5p
Atherosclerosis (AS) is a chronic inflammatory disease threatening human health, and vascular smooth muscle cells (VSMCs) are involved in AS processes. Baicalin is a flavonoid compound, which has anti-atherosclerotic effect. The aim of our study was to explore the molecular mechanism of baicalin on...
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| Veröffentlicht in: | Biological & pharmaceutical bulletin 2019/09/01, Vol.42(9), pp.1517-1523 |
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| creator | Chen, Zhongpu Pan, Xiaodong Sheng, Zulong Yan, Gaoliang Chen, Long Ma, Genshan |
| description | Atherosclerosis (AS) is a chronic inflammatory disease threatening human health, and vascular smooth muscle cells (VSMCs) are involved in AS processes. Baicalin is a flavonoid compound, which has anti-atherosclerotic effect. The aim of our study was to explore the molecular mechanism of baicalin on AS. The expression of miR-126-5p was measured in peripheral blood of AS patients and healthy control. We found miR-126-5p expression was decreased in AS. Then, high-mobility group box 1 (HMGB1) was verified as a target of miR-126-5p and its expression was increased in AS. Similarly, miR-126-5p and HMGB1 expression was downregulated and upregulated in oxidized low-density lipoprotein treated VSMCs (ox-LDL-VSMCs), respectively. Furthermore, baicalin upregulated miR-126-5p and downregulated HMGB1 expression. Functionally, baicalin significantly inhibited ox-LDL-VSMCs proliferation and migration, and miR-126-5p targets HMGB1 to enhance the inhibition induced by baicalin. Taken together, baicalin is able to prevent AS, which suppressed the proliferation and migration of ox-LDL-VSMCs through upregulating miR-126-5p by targeting HMGB1. These findings suggested that baicalin is an effective drug to alleviate AS, and miR-126-5p is a novel therapeutic target for AS. |
| doi_str_mv | 10.1248/bpb.b19-00196 |
| format | Article |
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Baicalin is a flavonoid compound, which has anti-atherosclerotic effect. The aim of our study was to explore the molecular mechanism of baicalin on AS. The expression of miR-126-5p was measured in peripheral blood of AS patients and healthy control. We found miR-126-5p expression was decreased in AS. Then, high-mobility group box 1 (HMGB1) was verified as a target of miR-126-5p and its expression was increased in AS. Similarly, miR-126-5p and HMGB1 expression was downregulated and upregulated in oxidized low-density lipoprotein treated VSMCs (ox-LDL-VSMCs), respectively. Furthermore, baicalin upregulated miR-126-5p and downregulated HMGB1 expression. Functionally, baicalin significantly inhibited ox-LDL-VSMCs proliferation and migration, and miR-126-5p targets HMGB1 to enhance the inhibition induced by baicalin. Taken together, baicalin is able to prevent AS, which suppressed the proliferation and migration of ox-LDL-VSMCs through upregulating miR-126-5p by targeting HMGB1. These findings suggested that baicalin is an effective drug to alleviate AS, and miR-126-5p is a novel therapeutic target for AS.</description><identifier>ISSN: 0918-6158</identifier><identifier>EISSN: 1347-5215</identifier><identifier>DOI: 10.1248/bpb.b19-00196</identifier><identifier>PMID: 31204352</identifier><language>eng</language><publisher>Japan: The Pharmaceutical Society of Japan</publisher><subject>Arteriosclerosis ; Atherosclerosis ; Atherosclerosis - genetics ; Baicalin ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Down-Regulation - drug effects ; Female ; Flavonoids ; Flavonoids - pharmacology ; Health risks ; high-mobility group box 1 (HMGB1) ; HMGB1 protein ; HMGB1 Protein - genetics ; HMGB1 Protein - metabolism ; Humans ; Inflammatory diseases ; Lipoproteins, LDL ; Low density lipoprotein ; Male ; MicroRNAs - biosynthesis ; MicroRNAs - genetics ; Middle Aged ; migration ; miR-126-5p ; Muscle, Smooth, Vascular - cytology ; Muscles ; Myocytes, Smooth Muscle - drug effects ; Myocytes, Smooth Muscle - physiology ; Peripheral blood ; proliferation ; Smooth muscle ; Therapeutic applications ; Up-Regulation - drug effects</subject><ispartof>Biological and Pharmaceutical Bulletin, 2019/09/01, Vol.42(9), pp.1517-1523</ispartof><rights>2019 The Pharmaceutical Society of Japan</rights><rights>Copyright Japan Science and Technology Agency 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c702t-7e43133336c2c6eeb964eecd936d55f5c2141266e7bc01b1334b4c346ff95c4f3</citedby><cites>FETCH-LOGICAL-c702t-7e43133336c2c6eeb964eecd936d55f5c2141266e7bc01b1334b4c346ff95c4f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1883,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31204352$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Zhongpu</creatorcontrib><creatorcontrib>Pan, Xiaodong</creatorcontrib><creatorcontrib>Sheng, Zulong</creatorcontrib><creatorcontrib>Yan, Gaoliang</creatorcontrib><creatorcontrib>Chen, Long</creatorcontrib><creatorcontrib>Ma, Genshan</creatorcontrib><creatorcontrib>Southeast University</creatorcontrib><creatorcontrib>The Department of Cardiology</creatorcontrib><creatorcontrib>Zhongda Hospital</creatorcontrib><title>Baicalin Suppresses the Proliferation and Migration of Ox-LDL-VSMCs in Atherosclerosis through Upregulating miR-126-5p</title><title>Biological & pharmaceutical bulletin</title><addtitle>Biol Pharm Bull</addtitle><description>Atherosclerosis (AS) is a chronic inflammatory disease threatening human health, and vascular smooth muscle cells (VSMCs) are involved in AS processes. Baicalin is a flavonoid compound, which has anti-atherosclerotic effect. The aim of our study was to explore the molecular mechanism of baicalin on AS. The expression of miR-126-5p was measured in peripheral blood of AS patients and healthy control. We found miR-126-5p expression was decreased in AS. Then, high-mobility group box 1 (HMGB1) was verified as a target of miR-126-5p and its expression was increased in AS. Similarly, miR-126-5p and HMGB1 expression was downregulated and upregulated in oxidized low-density lipoprotein treated VSMCs (ox-LDL-VSMCs), respectively. Furthermore, baicalin upregulated miR-126-5p and downregulated HMGB1 expression. Functionally, baicalin significantly inhibited ox-LDL-VSMCs proliferation and migration, and miR-126-5p targets HMGB1 to enhance the inhibition induced by baicalin. Taken together, baicalin is able to prevent AS, which suppressed the proliferation and migration of ox-LDL-VSMCs through upregulating miR-126-5p by targeting HMGB1. These findings suggested that baicalin is an effective drug to alleviate AS, and miR-126-5p is a novel therapeutic target for AS.</description><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - genetics</subject><subject>Baicalin</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Down-Regulation - drug effects</subject><subject>Female</subject><subject>Flavonoids</subject><subject>Flavonoids - pharmacology</subject><subject>Health risks</subject><subject>high-mobility group box 1 (HMGB1)</subject><subject>HMGB1 protein</subject><subject>HMGB1 Protein - genetics</subject><subject>HMGB1 Protein - metabolism</subject><subject>Humans</subject><subject>Inflammatory diseases</subject><subject>Lipoproteins, LDL</subject><subject>Low density lipoprotein</subject><subject>Male</subject><subject>MicroRNAs - biosynthesis</subject><subject>MicroRNAs - genetics</subject><subject>Middle Aged</subject><subject>migration</subject><subject>miR-126-5p</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Muscles</subject><subject>Myocytes, Smooth Muscle - drug effects</subject><subject>Myocytes, Smooth Muscle - physiology</subject><subject>Peripheral blood</subject><subject>proliferation</subject><subject>Smooth muscle</subject><subject>Therapeutic applications</subject><subject>Up-Regulation - drug effects</subject><issn>0918-6158</issn><issn>1347-5215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkU2P0zAQhi0EYsvCkSuKxIWLF38nOS4FFqSuFrEsV8txJ62rNA52guDfM2lLkfBhRtY8887YLyEvObviQlVvm6G5anhNGeO1eUQWXKqSasH1Y7JgNa-o4bq6IM9y3jHGSibkU3IhuWBKarEgP9-54F0X-uJ-GoYEOUMuxi0UX1LsQgvJjSH2hevXxW3YnG6xLe5-0dX7Ff1-f7vMBXZfY0-K2XdzDLNEitNmWzyg5mbqsK_fFPvwlXJhqB6ekyet6zK8OOVL8vDxw7flJ7q6u_m8vF5Rj5uOtAQlucRjvPAGoKmNAvDrWpq11q32gisUNFA2nvEGUdUoL5Vp21p71cpL8uaoO6T4Y4I82n3IHrrO9RCnbIWopKjKuioRff0fuotT6nE7pGrFhFGVRIoeKY_vzAlaO6Swd-m35czOhlg0xKIh9mAI8q9OqlOzh_WZ_usAAjdHAKuzE7FHM-DfbJ_LJsQuWsEOokowTJxbrnmJQcy_I6SuUGl5VNrl0W3gPMqlMaAvh8WUsPUczgueq37rkoVe_gHsGLPR</recordid><startdate>20190901</startdate><enddate>20190901</enddate><creator>Chen, Zhongpu</creator><creator>Pan, Xiaodong</creator><creator>Sheng, Zulong</creator><creator>Yan, Gaoliang</creator><creator>Chen, Long</creator><creator>Ma, Genshan</creator><general>The Pharmaceutical Society of Japan</general><general>Pharmaceutical Society of Japan</general><general>Japan Science and Technology Agency</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20190901</creationdate><title>Baicalin Suppresses the Proliferation and Migration of Ox-LDL-VSMCs in Atherosclerosis through Upregulating miR-126-5p</title><author>Chen, Zhongpu ; Pan, Xiaodong ; Sheng, Zulong ; Yan, Gaoliang ; Chen, Long ; Ma, Genshan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c702t-7e43133336c2c6eeb964eecd936d55f5c2141266e7bc01b1334b4c346ff95c4f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Arteriosclerosis</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis - genetics</topic><topic>Baicalin</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Down-Regulation - drug effects</topic><topic>Female</topic><topic>Flavonoids</topic><topic>Flavonoids - pharmacology</topic><topic>Health risks</topic><topic>high-mobility group box 1 (HMGB1)</topic><topic>HMGB1 protein</topic><topic>HMGB1 Protein - genetics</topic><topic>HMGB1 Protein - metabolism</topic><topic>Humans</topic><topic>Inflammatory diseases</topic><topic>Lipoproteins, LDL</topic><topic>Low density lipoprotein</topic><topic>Male</topic><topic>MicroRNAs - biosynthesis</topic><topic>MicroRNAs - genetics</topic><topic>Middle Aged</topic><topic>migration</topic><topic>miR-126-5p</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Muscles</topic><topic>Myocytes, Smooth Muscle - drug effects</topic><topic>Myocytes, Smooth Muscle - physiology</topic><topic>Peripheral blood</topic><topic>proliferation</topic><topic>Smooth muscle</topic><topic>Therapeutic applications</topic><topic>Up-Regulation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Zhongpu</creatorcontrib><creatorcontrib>Pan, Xiaodong</creatorcontrib><creatorcontrib>Sheng, Zulong</creatorcontrib><creatorcontrib>Yan, Gaoliang</creatorcontrib><creatorcontrib>Chen, Long</creatorcontrib><creatorcontrib>Ma, Genshan</creatorcontrib><creatorcontrib>Southeast University</creatorcontrib><creatorcontrib>The Department of Cardiology</creatorcontrib><creatorcontrib>Zhongda Hospital</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biological & pharmaceutical bulletin</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Zhongpu</au><au>Pan, Xiaodong</au><au>Sheng, Zulong</au><au>Yan, Gaoliang</au><au>Chen, Long</au><au>Ma, Genshan</au><aucorp>Southeast University</aucorp><aucorp>The Department of Cardiology</aucorp><aucorp>Zhongda Hospital</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Baicalin Suppresses the Proliferation and Migration of Ox-LDL-VSMCs in Atherosclerosis through Upregulating miR-126-5p</atitle><jtitle>Biological & pharmaceutical bulletin</jtitle><addtitle>Biol Pharm Bull</addtitle><date>2019-09-01</date><risdate>2019</risdate><volume>42</volume><issue>9</issue><spage>1517</spage><epage>1523</epage><pages>1517-1523</pages><issn>0918-6158</issn><eissn>1347-5215</eissn><abstract>Atherosclerosis (AS) is a chronic inflammatory disease threatening human health, and vascular smooth muscle cells (VSMCs) are involved in AS processes. Baicalin is a flavonoid compound, which has anti-atherosclerotic effect. The aim of our study was to explore the molecular mechanism of baicalin on AS. The expression of miR-126-5p was measured in peripheral blood of AS patients and healthy control. We found miR-126-5p expression was decreased in AS. Then, high-mobility group box 1 (HMGB1) was verified as a target of miR-126-5p and its expression was increased in AS. Similarly, miR-126-5p and HMGB1 expression was downregulated and upregulated in oxidized low-density lipoprotein treated VSMCs (ox-LDL-VSMCs), respectively. Furthermore, baicalin upregulated miR-126-5p and downregulated HMGB1 expression. Functionally, baicalin significantly inhibited ox-LDL-VSMCs proliferation and migration, and miR-126-5p targets HMGB1 to enhance the inhibition induced by baicalin. Taken together, baicalin is able to prevent AS, which suppressed the proliferation and migration of ox-LDL-VSMCs through upregulating miR-126-5p by targeting HMGB1. These findings suggested that baicalin is an effective drug to alleviate AS, and miR-126-5p is a novel therapeutic target for AS.</abstract><cop>Japan</cop><pub>The Pharmaceutical Society of Japan</pub><pmid>31204352</pmid><doi>10.1248/bpb.b19-00196</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Arteriosclerosis Atherosclerosis Atherosclerosis - genetics Baicalin Cell Movement - drug effects Cell Proliferation - drug effects Down-Regulation - drug effects Female Flavonoids Flavonoids - pharmacology Health risks high-mobility group box 1 (HMGB1) HMGB1 protein HMGB1 Protein - genetics HMGB1 Protein - metabolism Humans Inflammatory diseases Lipoproteins, LDL Low density lipoprotein Male MicroRNAs - biosynthesis MicroRNAs - genetics Middle Aged migration miR-126-5p Muscle, Smooth, Vascular - cytology Muscles Myocytes, Smooth Muscle - drug effects Myocytes, Smooth Muscle - physiology Peripheral blood proliferation Smooth muscle Therapeutic applications Up-Regulation - drug effects |
| title | Baicalin Suppresses the Proliferation and Migration of Ox-LDL-VSMCs in Atherosclerosis through Upregulating miR-126-5p |
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