Acteoside Derived from Cistanche Improves Glucocorticoid-Induced Osteoporosis by Activating PI3K/AKT/mTOR Pathway
Glucocorticoids are widely used in clinical practice; however, they can cause side effects, such as osteoporosis. Acteoside (ACT) from Cistanche has been used to combat a variety of diseases. The study was conducted to evaluate the efficacy of ACT in glucocorticoid-induced osteoporosis (GIOP) and it...
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| Veröffentlicht in: | Journal of investigative surgery 2023-12, Vol.36 (1), p.2154578-2154578 |
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| creator | Li, Shumei Cui, Yajie Li, Min Zhang, Wenting Sun, Xiaoxue Xin, Zhaoxu Li, Jing |
| description | Glucocorticoids are widely used in clinical practice; however, they can cause side effects, such as osteoporosis. Acteoside (ACT) from Cistanche has been used to combat a variety of diseases. The study was conducted to evaluate the efficacy of ACT in glucocorticoid-induced osteoporosis (GIOP) and its potential mechanism.
Dexamethasone (Dex) was injected intramuscularly to induce osteoporosis in a rat model, and ACT was given orally. ACT was supplemented in vivo in Dex-stimulated osteoblastic MC3T3-E1 cells. RT-qPCR was performed to assess the mRNA levels of bone formation (Runx2, CoL1A1), and bone resorption (OPG and RANKL). A commercial ELISA kit was applied to assess serum OC and CTX levels. Western blot was performed to assess protein levels in the PI3K/AKT/mTOR signaling pathway. CCK-8 assay and flow cytometry were performed to assess osteoblast viability and apoptosis.
ACT reduced Dex-induced bone microstructure deterioration, increased serum levels of OC, and decreased the levels of CTX (P |
| doi_str_mv | 10.1080/08941939.2022.2154578 |
| format | Article |
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Dexamethasone (Dex) was injected intramuscularly to induce osteoporosis in a rat model, and ACT was given orally. ACT was supplemented in vivo in Dex-stimulated osteoblastic MC3T3-E1 cells. RT-qPCR was performed to assess the mRNA levels of bone formation (Runx2, CoL1A1), and bone resorption (OPG and RANKL). A commercial ELISA kit was applied to assess serum OC and CTX levels. Western blot was performed to assess protein levels in the PI3K/AKT/mTOR signaling pathway. CCK-8 assay and flow cytometry were performed to assess osteoblast viability and apoptosis.
ACT reduced Dex-induced bone microstructure deterioration, increased serum levels of OC, and decreased the levels of CTX (P < 0.05). In the MC3T3-E1 cells, Dex inhibited cell viability and promoted apoptosis; however, this effect was greatly attenuated by ACT (P < 0.05). Concurrently, ACT reversed the reduction in Runx2, osterix, CoL1A1, and OPG mRNA levels, ALP activity, and the promotion of RANKL by Dex. Additionally, ACT attenuated Dex-induced inhibition of p-AKT/AKT, p-mTOR/mTOR, and p-PI3K/PI3K protein levels by Dex (P < 0.05), while the PI3K/AKT/mTOR pathway inhibitor LY294002 diminished the potential effect of ACT (P < 0.05).
ACT from Cistanche may exert osteoprotective effects by activating the PI3K/AKT/mTOR signaling pathway to alleviate Dex-induced osteoporosis.</description><identifier>ISSN: 0894-1939</identifier><identifier>EISSN: 1521-0553</identifier><identifier>DOI: 10.1080/08941939.2022.2154578</identifier><identifier>PMID: 36521840</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>Acteoside ; Animals ; Cistanche ; Cistanche - metabolism ; Core Binding Factor Alpha 1 Subunit - metabolism ; Core Binding Factor Alpha 1 Subunit - pharmacology ; Dexamethasone - adverse effects ; Glucocorticoids - adverse effects ; glucocorticoids-induced osteoporosis ; Osteoblasts ; Osteoporosis - chemically induced ; Osteoporosis - drug therapy ; Osteoporosis - prevention & control ; Phosphatidylinositol 3-Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; RNA, Messenger - metabolism ; TOR Serine-Threonine Kinases</subject><ispartof>Journal of investigative surgery, 2023-12, Vol.36 (1), p.2154578-2154578</ispartof><rights>2022 The Author(s). Published with license by Taylor & Francis Group, LLC 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c432t-9a3463f1a80264a709b3a02b8f47a04988ab030ce0b0f9a08ec40a7007662e5c3</citedby><cites>FETCH-LOGICAL-c432t-9a3463f1a80264a709b3a02b8f47a04988ab030ce0b0f9a08ec40a7007662e5c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.tandfonline.com/doi/pdf/10.1080/08941939.2022.2154578$$EPDF$$P50$$Ginformaworld$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.tandfonline.com/doi/full/10.1080/08941939.2022.2154578$$EHTML$$P50$$Ginformaworld$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,864,2102,27502,27924,27925,59143,59144</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36521840$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Shumei</creatorcontrib><creatorcontrib>Cui, Yajie</creatorcontrib><creatorcontrib>Li, Min</creatorcontrib><creatorcontrib>Zhang, Wenting</creatorcontrib><creatorcontrib>Sun, Xiaoxue</creatorcontrib><creatorcontrib>Xin, Zhaoxu</creatorcontrib><creatorcontrib>Li, Jing</creatorcontrib><title>Acteoside Derived from Cistanche Improves Glucocorticoid-Induced Osteoporosis by Activating PI3K/AKT/mTOR Pathway</title><title>Journal of investigative surgery</title><addtitle>J Invest Surg</addtitle><description>Glucocorticoids are widely used in clinical practice; however, they can cause side effects, such as osteoporosis. Acteoside (ACT) from Cistanche has been used to combat a variety of diseases. The study was conducted to evaluate the efficacy of ACT in glucocorticoid-induced osteoporosis (GIOP) and its potential mechanism.
Dexamethasone (Dex) was injected intramuscularly to induce osteoporosis in a rat model, and ACT was given orally. ACT was supplemented in vivo in Dex-stimulated osteoblastic MC3T3-E1 cells. RT-qPCR was performed to assess the mRNA levels of bone formation (Runx2, CoL1A1), and bone resorption (OPG and RANKL). A commercial ELISA kit was applied to assess serum OC and CTX levels. Western blot was performed to assess protein levels in the PI3K/AKT/mTOR signaling pathway. CCK-8 assay and flow cytometry were performed to assess osteoblast viability and apoptosis.
ACT reduced Dex-induced bone microstructure deterioration, increased serum levels of OC, and decreased the levels of CTX (P < 0.05). In the MC3T3-E1 cells, Dex inhibited cell viability and promoted apoptosis; however, this effect was greatly attenuated by ACT (P < 0.05). Concurrently, ACT reversed the reduction in Runx2, osterix, CoL1A1, and OPG mRNA levels, ALP activity, and the promotion of RANKL by Dex. Additionally, ACT attenuated Dex-induced inhibition of p-AKT/AKT, p-mTOR/mTOR, and p-PI3K/PI3K protein levels by Dex (P < 0.05), while the PI3K/AKT/mTOR pathway inhibitor LY294002 diminished the potential effect of ACT (P < 0.05).
ACT from Cistanche may exert osteoprotective effects by activating the PI3K/AKT/mTOR signaling pathway to alleviate Dex-induced osteoporosis.</description><subject>Acteoside</subject><subject>Animals</subject><subject>Cistanche</subject><subject>Cistanche - metabolism</subject><subject>Core Binding Factor Alpha 1 Subunit - metabolism</subject><subject>Core Binding Factor Alpha 1 Subunit - pharmacology</subject><subject>Dexamethasone - adverse effects</subject><subject>Glucocorticoids - adverse effects</subject><subject>glucocorticoids-induced osteoporosis</subject><subject>Osteoblasts</subject><subject>Osteoporosis - chemically induced</subject><subject>Osteoporosis - drug therapy</subject><subject>Osteoporosis - prevention & control</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>RNA, Messenger - metabolism</subject><subject>TOR Serine-Threonine Kinases</subject><issn>0894-1939</issn><issn>1521-0553</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>EIF</sourceid><sourceid>DOA</sourceid><recordid>eNp9kctu2zAQRYmiReOk_YQWWnYje8SHRO1quG0qJICDwl0TI4pKGEiiQ0oO_PelYifLrggMzpwLziXkSwbLDCSsQJY8K1m5pEDpkmaCi0K-I4tM0CwFIdh7spiZdIYuyGUIjwBAeck-kguWR0pyWJCntR6NC7YxyQ_j7cE0Setdn2xsGHHQDyap-r13BxOS627STjs_Wu1sk1ZDM-mIb0MU7J2PkpDUxyQK7QFHO9wndxW7Wa1vdqt-t_2T3OH48IzHT-RDi10wn8_vFfn76-du8zu93V5Xm_VtqjmjY1oi4zlrM5RAc44FlDVDoLVseYHASymxBgbaQA1tiSCN5hAxKPKcGqHZFalO3sbho9p726M_KodWvQycv1c4_6UzihUZClYXjKLmeZPLnFHDmuitS1lmPLq-nVzxFE-TCaPqbdCm63AwbgqKFkKIQjABERUnVMeLBG_at-gM1Nycem1Ozc2pc3Nx7-s5Yqp707xtvVYVge8nwA6t8z0-O981asRj53zrY1c2KPb_jH-0bqaB</recordid><startdate>20231231</startdate><enddate>20231231</enddate><creator>Li, Shumei</creator><creator>Cui, Yajie</creator><creator>Li, Min</creator><creator>Zhang, Wenting</creator><creator>Sun, Xiaoxue</creator><creator>Xin, Zhaoxu</creator><creator>Li, Jing</creator><general>Taylor & Francis</general><general>Taylor & Francis Group</general><scope>0YH</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>7X8</scope><scope>DOA</scope></search><sort><creationdate>20231231</creationdate><title>Acteoside Derived from Cistanche Improves Glucocorticoid-Induced Osteoporosis by Activating PI3K/AKT/mTOR Pathway</title><author>Li, Shumei ; Cui, Yajie ; Li, Min ; Zhang, Wenting ; Sun, Xiaoxue ; Xin, Zhaoxu ; Li, Jing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c432t-9a3463f1a80264a709b3a02b8f47a04988ab030ce0b0f9a08ec40a7007662e5c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Acteoside</topic><topic>Animals</topic><topic>Cistanche</topic><topic>Cistanche - metabolism</topic><topic>Core Binding Factor Alpha 1 Subunit - metabolism</topic><topic>Core Binding Factor Alpha 1 Subunit - pharmacology</topic><topic>Dexamethasone - adverse effects</topic><topic>Glucocorticoids - adverse effects</topic><topic>glucocorticoids-induced osteoporosis</topic><topic>Osteoblasts</topic><topic>Osteoporosis - chemically induced</topic><topic>Osteoporosis - drug therapy</topic><topic>Osteoporosis - prevention & control</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rats</topic><topic>RNA, Messenger - metabolism</topic><topic>TOR Serine-Threonine Kinases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Shumei</creatorcontrib><creatorcontrib>Cui, Yajie</creatorcontrib><creatorcontrib>Li, Min</creatorcontrib><creatorcontrib>Zhang, Wenting</creatorcontrib><creatorcontrib>Sun, Xiaoxue</creatorcontrib><creatorcontrib>Xin, Zhaoxu</creatorcontrib><creatorcontrib>Li, Jing</creatorcontrib><collection>Taylor & Francis Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Journal of investigative surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Shumei</au><au>Cui, Yajie</au><au>Li, Min</au><au>Zhang, Wenting</au><au>Sun, Xiaoxue</au><au>Xin, Zhaoxu</au><au>Li, Jing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acteoside Derived from Cistanche Improves Glucocorticoid-Induced Osteoporosis by Activating PI3K/AKT/mTOR Pathway</atitle><jtitle>Journal of investigative surgery</jtitle><addtitle>J Invest Surg</addtitle><date>2023-12-31</date><risdate>2023</risdate><volume>36</volume><issue>1</issue><spage>2154578</spage><epage>2154578</epage><pages>2154578-2154578</pages><issn>0894-1939</issn><eissn>1521-0553</eissn><abstract>Glucocorticoids are widely used in clinical practice; however, they can cause side effects, such as osteoporosis. Acteoside (ACT) from Cistanche has been used to combat a variety of diseases. The study was conducted to evaluate the efficacy of ACT in glucocorticoid-induced osteoporosis (GIOP) and its potential mechanism.
Dexamethasone (Dex) was injected intramuscularly to induce osteoporosis in a rat model, and ACT was given orally. ACT was supplemented in vivo in Dex-stimulated osteoblastic MC3T3-E1 cells. RT-qPCR was performed to assess the mRNA levels of bone formation (Runx2, CoL1A1), and bone resorption (OPG and RANKL). A commercial ELISA kit was applied to assess serum OC and CTX levels. Western blot was performed to assess protein levels in the PI3K/AKT/mTOR signaling pathway. CCK-8 assay and flow cytometry were performed to assess osteoblast viability and apoptosis.
ACT reduced Dex-induced bone microstructure deterioration, increased serum levels of OC, and decreased the levels of CTX (P < 0.05). In the MC3T3-E1 cells, Dex inhibited cell viability and promoted apoptosis; however, this effect was greatly attenuated by ACT (P < 0.05). Concurrently, ACT reversed the reduction in Runx2, osterix, CoL1A1, and OPG mRNA levels, ALP activity, and the promotion of RANKL by Dex. Additionally, ACT attenuated Dex-induced inhibition of p-AKT/AKT, p-mTOR/mTOR, and p-PI3K/PI3K protein levels by Dex (P < 0.05), while the PI3K/AKT/mTOR pathway inhibitor LY294002 diminished the potential effect of ACT (P < 0.05).
ACT from Cistanche may exert osteoprotective effects by activating the PI3K/AKT/mTOR signaling pathway to alleviate Dex-induced osteoporosis.</abstract><cop>United States</cop><pub>Taylor & Francis</pub><pmid>36521840</pmid><doi>10.1080/08941939.2022.2154578</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acteoside Animals Cistanche Cistanche - metabolism Core Binding Factor Alpha 1 Subunit - metabolism Core Binding Factor Alpha 1 Subunit - pharmacology Dexamethasone - adverse effects Glucocorticoids - adverse effects glucocorticoids-induced osteoporosis Osteoblasts Osteoporosis - chemically induced Osteoporosis - drug therapy Osteoporosis - prevention & control Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Rats RNA, Messenger - metabolism TOR Serine-Threonine Kinases |
| title | Acteoside Derived from Cistanche Improves Glucocorticoid-Induced Osteoporosis by Activating PI3K/AKT/mTOR Pathway |
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