Compound from Magnolia officinalis Ameliorates White Matter Injury by Promoting Oligodendrocyte Maturation in Chronic Cerebral Ischemia Models
Chronic cerebral hypoperfusion leads to white matter injury (WMI), which subsequently causes neurodegeneration and even cognitive impairment. However, due to the lack of treatment specifically for WMI, novel recognized and effective therapeutic strategies are urgently needed. In this study, we found...
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| Veröffentlicht in: | Neuroscience bulletin 2023-10, Vol.39 (10), p.1497-1511 |
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| creator | Zhang, Zhi Shu, Xin Cao, Qian Xu, Lushan Wang, Zibu Li, Chenggang Xia, Shengnan Shao, Pengfei Bao, Xinyu Sun, Liang Xu, Yuhao Xu, Yun |
| description | Chronic cerebral hypoperfusion leads to white matter injury (WMI), which subsequently causes neurodegeneration and even cognitive impairment. However, due to the lack of treatment specifically for WMI, novel recognized and effective therapeutic strategies are urgently needed. In this study, we found that honokiol and magnolol, two compounds derived from
Magnolia officinalis
, significantly facilitated the differentiation of primary oligodendrocyte precursor cells (OPCs) into mature oligodendrocytes, with a more prominent effect of the former compound. Moreover, our results demonstrated that honokiol treatment improved myelin injury, induced mature oligodendrocyte protein expression, attenuated cognitive decline, promoted oligodendrocyte regeneration, and inhibited astrocytic activation in the bilateral carotid artery stenosis model. Mechanistically, honokiol increased the phosphorylation of serine/threonine kinase (Akt) and mammalian target of rapamycin (mTOR) by activating cannabinoid receptor 1 during OPC differentiation. Collectively, our study indicates that honokiol might serve as a potential treatment for WMI in chronic cerebral ischemia. |
| doi_str_mv | 10.1007/s12264-023-01068-z |
| format | Article |
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Magnolia officinalis
, significantly facilitated the differentiation of primary oligodendrocyte precursor cells (OPCs) into mature oligodendrocytes, with a more prominent effect of the former compound. Moreover, our results demonstrated that honokiol treatment improved myelin injury, induced mature oligodendrocyte protein expression, attenuated cognitive decline, promoted oligodendrocyte regeneration, and inhibited astrocytic activation in the bilateral carotid artery stenosis model. Mechanistically, honokiol increased the phosphorylation of serine/threonine kinase (Akt) and mammalian target of rapamycin (mTOR) by activating cannabinoid receptor 1 during OPC differentiation. Collectively, our study indicates that honokiol might serve as a potential treatment for WMI in chronic cerebral ischemia.</description><identifier>ISSN: 1673-7067</identifier><identifier>EISSN: 1995-8218</identifier><identifier>DOI: 10.1007/s12264-023-01068-z</identifier><identifier>PMID: 37291477</identifier><language>eng</language><publisher>Singapore: Springer Nature Singapore</publisher><subject>Anatomy ; Anesthesiology ; Biomedical and Life Sciences ; Biomedicine ; Human Physiology ; Neurology ; Neurosciences ; Original ; Original Article ; Pain Medicine</subject><ispartof>Neuroscience bulletin, 2023-10, Vol.39 (10), p.1497-1511</ispartof><rights>The Author(s) 2023</rights><rights>2023. The Author(s).</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c447t-f85667d52d9ca4494966dcb4cf1707200b7782ae004f39738bd8ddecd4c4e3d43</citedby><cites>FETCH-LOGICAL-c447t-f85667d52d9ca4494966dcb4cf1707200b7782ae004f39738bd8ddecd4c4e3d43</cites><orcidid>0000-0001-5288-0319</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/PMC10533772/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10533772/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37291477$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Zhi</creatorcontrib><creatorcontrib>Shu, Xin</creatorcontrib><creatorcontrib>Cao, Qian</creatorcontrib><creatorcontrib>Xu, Lushan</creatorcontrib><creatorcontrib>Wang, Zibu</creatorcontrib><creatorcontrib>Li, Chenggang</creatorcontrib><creatorcontrib>Xia, Shengnan</creatorcontrib><creatorcontrib>Shao, Pengfei</creatorcontrib><creatorcontrib>Bao, Xinyu</creatorcontrib><creatorcontrib>Sun, Liang</creatorcontrib><creatorcontrib>Xu, Yuhao</creatorcontrib><creatorcontrib>Xu, Yun</creatorcontrib><title>Compound from Magnolia officinalis Ameliorates White Matter Injury by Promoting Oligodendrocyte Maturation in Chronic Cerebral Ischemia Models</title><title>Neuroscience bulletin</title><addtitle>Neurosci. Bull</addtitle><addtitle>Neurosci Bull</addtitle><description>Chronic cerebral hypoperfusion leads to white matter injury (WMI), which subsequently causes neurodegeneration and even cognitive impairment. However, due to the lack of treatment specifically for WMI, novel recognized and effective therapeutic strategies are urgently needed. In this study, we found that honokiol and magnolol, two compounds derived from
Magnolia officinalis
, significantly facilitated the differentiation of primary oligodendrocyte precursor cells (OPCs) into mature oligodendrocytes, with a more prominent effect of the former compound. Moreover, our results demonstrated that honokiol treatment improved myelin injury, induced mature oligodendrocyte protein expression, attenuated cognitive decline, promoted oligodendrocyte regeneration, and inhibited astrocytic activation in the bilateral carotid artery stenosis model. Mechanistically, honokiol increased the phosphorylation of serine/threonine kinase (Akt) and mammalian target of rapamycin (mTOR) by activating cannabinoid receptor 1 during OPC differentiation. Collectively, our study indicates that honokiol might serve as a potential treatment for WMI in chronic cerebral ischemia.</description><subject>Anatomy</subject><subject>Anesthesiology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Human Physiology</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Original</subject><subject>Original Article</subject><subject>Pain Medicine</subject><issn>1673-7067</issn><issn>1995-8218</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><recordid>eNp9kctu1DAUhiMEoqXwAiyQl2wCvsV2VqiKuIzUqixALC3HPsl4lNiDnVSaPgTPjCGlgg0rWzrf_58jfVX1kuA3BGP5NhNKBa8xZTUmWKj67lF1Ttq2qRUl6nH5C8lqiYU8q57lfMBYYMn40-qMSdoSLuV59aOL8zGuwaEhxRldmzHEyRsUh8FbH8zkM7qcYfIxmQUy-rb3CxRsWSChXTis6YT6E_pcwnHxYUQ3kx-jg-BStKcNXUvUx4B8QN0-xeAt6iBBn8yEdtnuYS4Lr0toys-rJ4OZMry4fy-qrx_ef-k-1Vc3H3fd5VVtOZdLPahGCOka6lprOG95K4SzPbcDkVhSjHspFTWAMR9YK5nqnXIOrOOWA3OcXVTvtt7j2s_gLISlXKOPyc8mnXQ0Xv87CX6vx3irCW4Yk5KWhtf3DSl-XyEvevbZwjSZAHHNmirKhRKkkQWlG2pTzDnB8LCHYP3LpN5M6mJS_zap70ro1d8XPkT-qCsA24BcRmGEpA9xTcVY_l_tT1Ryrm8</recordid><startdate>20231001</startdate><enddate>20231001</enddate><creator>Zhang, Zhi</creator><creator>Shu, Xin</creator><creator>Cao, Qian</creator><creator>Xu, Lushan</creator><creator>Wang, Zibu</creator><creator>Li, Chenggang</creator><creator>Xia, Shengnan</creator><creator>Shao, Pengfei</creator><creator>Bao, Xinyu</creator><creator>Sun, Liang</creator><creator>Xu, Yuhao</creator><creator>Xu, Yun</creator><general>Springer Nature Singapore</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-5288-0319</orcidid></search><sort><creationdate>20231001</creationdate><title>Compound from Magnolia officinalis Ameliorates White Matter Injury by Promoting Oligodendrocyte Maturation in Chronic Cerebral Ischemia Models</title><author>Zhang, Zhi ; Shu, Xin ; Cao, Qian ; Xu, Lushan ; Wang, Zibu ; Li, Chenggang ; Xia, Shengnan ; Shao, Pengfei ; Bao, Xinyu ; Sun, Liang ; Xu, Yuhao ; Xu, Yun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-f85667d52d9ca4494966dcb4cf1707200b7782ae004f39738bd8ddecd4c4e3d43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Anatomy</topic><topic>Anesthesiology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Human Physiology</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Original</topic><topic>Original Article</topic><topic>Pain Medicine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Zhi</creatorcontrib><creatorcontrib>Shu, Xin</creatorcontrib><creatorcontrib>Cao, Qian</creatorcontrib><creatorcontrib>Xu, Lushan</creatorcontrib><creatorcontrib>Wang, Zibu</creatorcontrib><creatorcontrib>Li, Chenggang</creatorcontrib><creatorcontrib>Xia, Shengnan</creatorcontrib><creatorcontrib>Shao, Pengfei</creatorcontrib><creatorcontrib>Bao, Xinyu</creatorcontrib><creatorcontrib>Sun, Liang</creatorcontrib><creatorcontrib>Xu, Yuhao</creatorcontrib><creatorcontrib>Xu, Yun</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neuroscience bulletin</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Zhi</au><au>Shu, Xin</au><au>Cao, Qian</au><au>Xu, Lushan</au><au>Wang, Zibu</au><au>Li, Chenggang</au><au>Xia, Shengnan</au><au>Shao, Pengfei</au><au>Bao, Xinyu</au><au>Sun, Liang</au><au>Xu, Yuhao</au><au>Xu, Yun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Compound from Magnolia officinalis Ameliorates White Matter Injury by Promoting Oligodendrocyte Maturation in Chronic Cerebral Ischemia Models</atitle><jtitle>Neuroscience bulletin</jtitle><stitle>Neurosci. Bull</stitle><addtitle>Neurosci Bull</addtitle><date>2023-10-01</date><risdate>2023</risdate><volume>39</volume><issue>10</issue><spage>1497</spage><epage>1511</epage><pages>1497-1511</pages><issn>1673-7067</issn><eissn>1995-8218</eissn><abstract>Chronic cerebral hypoperfusion leads to white matter injury (WMI), which subsequently causes neurodegeneration and even cognitive impairment. However, due to the lack of treatment specifically for WMI, novel recognized and effective therapeutic strategies are urgently needed. In this study, we found that honokiol and magnolol, two compounds derived from
Magnolia officinalis
, significantly facilitated the differentiation of primary oligodendrocyte precursor cells (OPCs) into mature oligodendrocytes, with a more prominent effect of the former compound. Moreover, our results demonstrated that honokiol treatment improved myelin injury, induced mature oligodendrocyte protein expression, attenuated cognitive decline, promoted oligodendrocyte regeneration, and inhibited astrocytic activation in the bilateral carotid artery stenosis model. Mechanistically, honokiol increased the phosphorylation of serine/threonine kinase (Akt) and mammalian target of rapamycin (mTOR) by activating cannabinoid receptor 1 during OPC differentiation. Collectively, our study indicates that honokiol might serve as a potential treatment for WMI in chronic cerebral ischemia.</abstract><cop>Singapore</cop><pub>Springer Nature Singapore</pub><pmid>37291477</pmid><doi>10.1007/s12264-023-01068-z</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0001-5288-0319</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Anatomy Anesthesiology Biomedical and Life Sciences Biomedicine Human Physiology Neurology Neurosciences Original Original Article Pain Medicine |
| title | Compound from Magnolia officinalis Ameliorates White Matter Injury by Promoting Oligodendrocyte Maturation in Chronic Cerebral Ischemia Models |
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