Artemisia annua L. extract regulates bone-fat metabolism on glucocorticoid-induced osteoporosis via regulating PGC-1α/Nrf2-mediated oxidative stress

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Abstract Artemisia annua L. is a well-known traditional herb medicine, and possesses antioxidant, antiobesity and antiosteoporosis properties. This paper aimed to explore the role and mechanism of Artemisia annua L. on glucocorticoid-induced osteoporosis (GIOP). Artemisia annua L. extract (AE) improved bone mineral density (BMD) and micro-architectural parameters in GIOP mice femur. Biological indicators showed that AE protected bone formation and inhibited fat formation in GIOP mice, and the potential mechanism was regulating oxidative stress (OS) via promoting the nuclear expression of Nrf2. To further investigate the mechanism of AE on GIOP, MC3T3-E1 cells injured by dexamethasone (DEX) were used for in vitro study. AE promoted proliferation and mineralization, upregulated the expression of Runx2, and downregulated the expression of PPARγ in DEX-injured MC3T3-E1 cells. In addition, AE reduced the level of oxidative factors and promoted the level of antioxidant enzymes in DEX-injured MC3T3-E1 cells. Western blot showed that AE activated the PGC-1α/Nrf2 pathway, which may be the potential mechanism of AE playing antioxidant role. Furthermore, PGC-1α or Nrf2 knockdown by siRNA reversed the antioxidant effect of AE. These results revealed that AE exerts anti-GIOP effects via egulating bone-fat metabolism via regulating PGC-1α/Nrf2-mediated OS.
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Artemisia annua L. extract regulates bone-fat metabolism on glucocorticoid-induced osteoporosis via regulating PGC-1α/Nrf2-mediated oxidative stress | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Artemisia annua L. extract regulates bone-fat metabolism on glucocorticoid-induced osteoporosis via regulating PGC-1α/Nrf2-mediated oxidative stress Liyong Lai, Tianshuang Xia, Luying Ding, Kun Li, Shengyan Xu, and 4 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-4667927/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Artemisia annua L. is a well-known traditional herb medicine, and possesses antioxidant, antiobesity and antiosteoporosis properties. This paper aimed to explore the role and mechanism of Artemisia annua L. on glucocorticoid-induced osteoporosis (GIOP). Artemisia annua L. extract (AE) improved bone mineral density (BMD) and micro-architectural parameters in GIOP mice femur. Biological indicators showed that AE protected bone formation and inhibited fat formation in GIOP mice, and the potential mechanism was regulating oxidative stress (OS) via promoting the nuclear expression of Nrf2. To further investigate the mechanism of AE on GIOP, MC3T3-E1 cells injured by dexamethasone (DEX) were used for in vitro study. AE promoted proliferation and mineralization, upregulated the expression of Runx2, and downregulated the expression of PPARγ in DEX-injured MC3T3-E1 cells. In addition, AE reduced the level of oxidative factors and promoted the level of antioxidant enzymes in DEX-injured MC3T3-E1 cells. Western blot showed that AE activated the PGC-1α/Nrf2 pathway, which may be the potential mechanism of AE playing antioxidant role. Furthermore, PGC-1α or Nrf2 knockdown by siRNA reversed the antioxidant effect of AE. These results revealed that AE exerts anti-GIOP effects via egulating bone-fat metabolism via regulating PGC-1α/Nrf2-mediated OS. Artemisia annua L. bone-fat metabolism glucocorticoid-induced osteoporosis oxidative stress PGC-1α/Nrf2 Full Text Additional Declarations No competing interests reported. Supplementary Files Additionalfle1.docx Additional file 1: Figure S1. IHPLC for AE and reference substances. Figure S2. Ultraviolet spectrum of 11 constituents in AE. Figure S3. Ultraviolet spectrum of 11 constituents in reference substances. graphicalabstract.tif Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-4667927","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":321627281,"identity":"bf3a0546-1c75-40fb-92fe-e6cc1cf28c67","order_by":0,"name":"Liyong Lai","email":"","orcid":"","institution":"Naval Medical University","correspondingAuthor":false,"prefix":"","firstName":"Liyong","middleName":"","lastName":"Lai","suffix":""},{"id":321627282,"identity":"5cb7b0a1-b135-42fb-8f2d-13e1d1a4cadc","order_by":1,"name":"Tianshuang Xia","email":"","orcid":"","institution":"Naval Medical University","correspondingAuthor":false,"prefix":"","firstName":"Tianshuang","middleName":"","lastName":"Xia","suffix":""},{"id":321627283,"identity":"c0930fd2-9c74-4ce3-a15f-ae931189ec8a","order_by":2,"name":"Luying Ding","email":"","orcid":"","institution":"The First Affiliated Hospital of Naval Medical University","correspondingAuthor":false,"prefix":"","firstName":"Luying","middleName":"","lastName":"Ding","suffix":""},{"id":321627284,"identity":"60318da2-1813-43d3-aeed-51fdc484c829","order_by":3,"name":"Kun Li","email":"","orcid":"","institution":"Naval Medical University","correspondingAuthor":false,"prefix":"","firstName":"Kun","middleName":"","lastName":"Li","suffix":""},{"id":321627285,"identity":"c0eb3352-0d54-480b-9312-241f85599695","order_by":4,"name":"Shengyan Xu","email":"","orcid":"","institution":"Naval Medical University","correspondingAuthor":false,"prefix":"","firstName":"Shengyan","middleName":"","lastName":"Xu","suffix":""},{"id":321627286,"identity":"9eeb7d1a-678f-4ff5-82d5-d23060447865","order_by":5,"name":"Yiping Jiang","email":"","orcid":"","institution":"Naval Medical University","correspondingAuthor":false,"prefix":"","firstName":"Yiping","middleName":"","lastName":"Jiang","suffix":""},{"id":321627287,"identity":"eb219514-4394-4a68-86ef-f3b3d0995c59","order_by":6,"name":"Weiqing Fan","email":"","orcid":"","institution":"Naval Medical University","correspondingAuthor":false,"prefix":"","firstName":"Weiqing","middleName":"","lastName":"Fan","suffix":""},{"id":321627288,"identity":"883e48f8-6f3b-45d9-8f28-80d03b54bc68","order_by":7,"name":"Xiaoqiang Yue","email":"","orcid":"","institution":"The Second Affiliated Hospital of Naval Medical University","correspondingAuthor":false,"prefix":"","firstName":"Xiaoqiang","middleName":"","lastName":"Yue","suffix":""},{"id":321627289,"identity":"da40500a-0430-4388-91ab-379e2f98efa6","order_by":8,"name":"Hailiang Xin","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA3ElEQVRIiWNgGAWjYBACAwbGxgMJIBYzA+ODhIoaorQ0wLQwGzw4c4wYLQwMB6BsNsmHLcyEtZizH2448KDmjt2G47zHKhIb2Bj427sT8Gqx7EkEOuzYs+SZzXxpNxJ3yDBInDm7Ab/DDoC0sB1O5mfmMbuReIaNwUAil4CW8w+BWv4dTmYDailIbGMmQssNoC2JbYftQLYwEKkFaEti3+EEyWYeY4mEM8d4CPvlfPrDhz++HbY3OH/G8OOPiho5/vZe/FpgILEByuAhSjkI2BOtchSMglEwCkYeAACQ2lANpvQXsQAAAABJRU5ErkJggg==","orcid":"","institution":"Naval Medical University","correspondingAuthor":true,"prefix":"","firstName":"Hailiang","middleName":"","lastName":"Xin","suffix":""}],"badges":[],"createdAt":"2024-07-01 12:06:29","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-4667927/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-4667927/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":61529667,"identity":"2e549dbd-edfd-49af-99b4-f167b3f6d696","added_by":"auto","created_at":"2024-07-31 22:06:32","extension":"pdf","order_by":1,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1511817,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-4667927/v1_covered_40965019-e02c-4cfb-bd48-cfe5f5c66edb.pdf"},{"id":60995757,"identity":"bcbe439d-c69e-44ca-87bf-86999d1aa89e","added_by":"auto","created_at":"2024-07-24 12:10:16","extension":"docx","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":425593,"visible":true,"origin":"","legend":"\u003cp\u003eAdditional file 1: Figure S1. 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