Proteomics-Guided Study on Buyang Huanwu Decoction for Its Neuroprotective and Neurogenic Mechanisms for Transient Ischemic Stroke: Involvements of EGFR/PI3K/Akt/Bad/14-3-3 and Jak2/Stat3/Cyclin D1 Signaling Cascades
Buyang Huanwu Decoction (BHD), a classic traditional Chinese medicine (TCM) formula, has been used for recovering neurological dysfunctions and treating post-stroke disability in China for 200 years. In the present study, we investigated the effects of BHD on inhibiting neuronal apoptosis, promoting...
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| description | Buyang Huanwu Decoction (BHD), a classic traditional Chinese medicine (TCM) formula, has been used for recovering neurological dysfunctions and treating post-stroke disability in China for 200 years. In the present study, we investigated the effects of BHD on inhibiting neuronal apoptosis, promoting proliferation and differentiation of neural stem cells (NSCs) and neurite formation and enhancing learning and memory functional recovery in an experimental rat ischemic stroke model. BHD significantly reduced infarct volume and decreased cell apoptosis in the ischemic brain. BHD enhanced neuronal cell viability in vitro. BHD dose-dependently promoted the proliferation of NSCs in ischemic rat brains in vivo. Moreover, BHD promoted neuronal and astrocyte differentiation in primary cultured NSCs in vitro. Water maze test revealed that BHD promoted the recovery of learning function but not memory functions in the transient ischemic rats. We then investigated the changes of the cellular signaling molecules by using two-dimension (2D) gel electrophoresis and focused on the PI3K/Akt/Bad and Jak2/Stat3/cyclin D1signaling pathway to uncover its underlying mechanisms for its neuroprotective and neurogenetic effects. BHD significantly upregulated the expression of p-PI3K, p-Akt, and p-Bad as well as the expression of p-Jak, p-Stat3, and cyclin D1 in vitro and in vivo. In addition, BHD upregulated Hes1 and downregulated cav-1
in vitro
and in vivo. Taken together, these results suggest that BHD has neuroprotective effects and neurogenesis-promoting effects via activating PI3K/Akt/Bad and Jak2/Stat3/Cyclin D1 signaling pathways.
Graphical Abstract
Buyang Huanwu Decoction (BHD) activates the PI3K-AKT-BAD pathway in the ischemic brain for neuroprotection. BHD also activates JAK2/STAT3/Cyclin D1 signaling cascades for promoting neurogenesis in the hippocampus of post-ischemic brains. Moreover, BHD inhibits the expression of caveolin-1 and increases the expression of HES1 for promoting neuronal differentiation. The neuroprotective and neurogenesis-promoting effects in the hippocampus of post-ischemic brains promote learning ability. |
| doi_str_mv | 10.1007/s12035-020-02016-y |
| format | Article |
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in vitro
and in vivo. Taken together, these results suggest that BHD has neuroprotective effects and neurogenesis-promoting effects via activating PI3K/Akt/Bad and Jak2/Stat3/Cyclin D1 signaling pathways.
Graphical Abstract
Buyang Huanwu Decoction (BHD) activates the PI3K-AKT-BAD pathway in the ischemic brain for neuroprotection. BHD also activates JAK2/STAT3/Cyclin D1 signaling cascades for promoting neurogenesis in the hippocampus of post-ischemic brains. Moreover, BHD inhibits the expression of caveolin-1 and increases the expression of HES1 for promoting neuronal differentiation. The neuroprotective and neurogenesis-promoting effects in the hippocampus of post-ischemic brains promote learning ability.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-020-02016-y</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>1-Phosphatidylinositol 3-kinase ; 14-3-3 protein ; AKT protein ; Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Caveolin-1 ; Cell Biology ; Cell differentiation ; Cell proliferation ; Cyclin D1 ; Epidermal growth factor receptors ; Gel electrophoresis ; Ischemia ; Janus kinase 2 ; Learning ; Neural stem cells ; Neurobiology ; Neurogenesis ; Neurological diseases ; Neurology ; Neuroprotection ; Neurosciences ; Original Article ; Proteomics ; Recovery of function ; Signal transduction ; Stat3 protein ; Stem cell transplantation ; Stem cells ; Stroke</subject><ispartof>Molecular neurobiology, 2020-10, Vol.57 (10), p.4305-4321</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c418t-2869af2f69819ac197b2547a223f2d1ba4e2bac4d331b9de588c2af39eaa59ab3</citedby><cites>FETCH-LOGICAL-c418t-2869af2f69819ac197b2547a223f2d1ba4e2bac4d331b9de588c2af39eaa59ab3</cites><orcidid>0000-0002-4199-8095</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-020-02016-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-020-02016-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids></links><search><creatorcontrib>Chen, Xi</creatorcontrib><creatorcontrib>Chen, Hansen</creatorcontrib><creatorcontrib>He, Yachong</creatorcontrib><creatorcontrib>Fu, Shuping</creatorcontrib><creatorcontrib>Liu, Haosheng</creatorcontrib><creatorcontrib>Wang, Qi</creatorcontrib><creatorcontrib>Shen, Jiangang</creatorcontrib><title>Proteomics-Guided Study on Buyang Huanwu Decoction for Its Neuroprotective and Neurogenic Mechanisms for Transient Ischemic Stroke: Involvements of EGFR/PI3K/Akt/Bad/14-3-3 and Jak2/Stat3/Cyclin D1 Signaling Cascades</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><description>Buyang Huanwu Decoction (BHD), a classic traditional Chinese medicine (TCM) formula, has been used for recovering neurological dysfunctions and treating post-stroke disability in China for 200 years. In the present study, we investigated the effects of BHD on inhibiting neuronal apoptosis, promoting proliferation and differentiation of neural stem cells (NSCs) and neurite formation and enhancing learning and memory functional recovery in an experimental rat ischemic stroke model. BHD significantly reduced infarct volume and decreased cell apoptosis in the ischemic brain. BHD enhanced neuronal cell viability in vitro. BHD dose-dependently promoted the proliferation of NSCs in ischemic rat brains in vivo. Moreover, BHD promoted neuronal and astrocyte differentiation in primary cultured NSCs in vitro. Water maze test revealed that BHD promoted the recovery of learning function but not memory functions in the transient ischemic rats. We then investigated the changes of the cellular signaling molecules by using two-dimension (2D) gel electrophoresis and focused on the PI3K/Akt/Bad and Jak2/Stat3/cyclin D1signaling pathway to uncover its underlying mechanisms for its neuroprotective and neurogenetic effects. BHD significantly upregulated the expression of p-PI3K, p-Akt, and p-Bad as well as the expression of p-Jak, p-Stat3, and cyclin D1 in vitro and in vivo. In addition, BHD upregulated Hes1 and downregulated cav-1
in vitro
and in vivo. Taken together, these results suggest that BHD has neuroprotective effects and neurogenesis-promoting effects via activating PI3K/Akt/Bad and Jak2/Stat3/Cyclin D1 signaling pathways.
Graphical Abstract
Buyang Huanwu Decoction (BHD) activates the PI3K-AKT-BAD pathway in the ischemic brain for neuroprotection. BHD also activates JAK2/STAT3/Cyclin D1 signaling cascades for promoting neurogenesis in the hippocampus of post-ischemic brains. Moreover, BHD inhibits the expression of caveolin-1 and increases the expression of HES1 for promoting neuronal differentiation. The neuroprotective and neurogenesis-promoting effects in the hippocampus of post-ischemic brains promote learning ability.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>14-3-3 protein</subject><subject>AKT protein</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Caveolin-1</subject><subject>Cell Biology</subject><subject>Cell differentiation</subject><subject>Cell proliferation</subject><subject>Cyclin D1</subject><subject>Epidermal growth factor receptors</subject><subject>Gel electrophoresis</subject><subject>Ischemia</subject><subject>Janus kinase 2</subject><subject>Learning</subject><subject>Neural stem cells</subject><subject>Neurobiology</subject><subject>Neurogenesis</subject><subject>Neurological diseases</subject><subject>Neurology</subject><subject>Neuroprotection</subject><subject>Neurosciences</subject><subject>Original Article</subject><subject>Proteomics</subject><subject>Recovery of function</subject><subject>Signal transduction</subject><subject>Stat3 protein</subject><subject>Stem cell transplantation</subject><subject>Stem cells</subject><subject>Stroke</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc1u1DAUhSMEEsPAC7CyxIZNiH_yZ3bttJ0GClRMWUc3zk2aTsZu7WRQ3pTHwZkgIbFgYdk6_s49lk8QvGX0A6M0ixzjVCQh5XReLA2nZ8GKJYkMGcv582BFcynCLI3zl8Er5x4o5ZzRbBX8urVmQHPolAu3Y1djTXbDWE_EaHI-TqBbcj2C_jmSC1RGDZ3XG2NJMTjyFUdrHme_149IQNeL1qLuFPmC6h505w7u5LizoF2HeiCFU_foE32SNXv8SAp9NP0RD_7SEdOQy-3V9-i2EJ-js_0QnUMdsTgUoTglfII9j3YDDCLaTKrvNLlgZNe1Gvy5JRtwCmp0r4MXDfQO3_zZ18GPq8u7zXV4821bbM5uQhWzfAh5nkpoeJPKnElQTGYVT-IMOBcNr1kFMfIKVFwLwSpZY5LnikMjJAIkEiqxDt4vc_1HPI3ohvLQOYV9DxrN6Eoe8zQR-dzPOnj3D_pgRuvfPVNCJixO89hTfKGUNc5ZbMpH2x3ATiWj5Vx2uZRd-qLLU9nl5E1iMTkP6xbt39H_cf0GfFiugg</recordid><startdate>20201001</startdate><enddate>20201001</enddate><creator>Chen, Xi</creator><creator>Chen, Hansen</creator><creator>He, Yachong</creator><creator>Fu, Shuping</creator><creator>Liu, Haosheng</creator><creator>Wang, Qi</creator><creator>Shen, Jiangang</creator><general>Springer US</general><general>Springer Nature 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Study on Buyang Huanwu Decoction for Its Neuroprotective and Neurogenic Mechanisms for Transient Ischemic Stroke: Involvements of EGFR/PI3K/Akt/Bad/14-3-3 and Jak2/Stat3/Cyclin D1 Signaling Cascades</title><author>Chen, Xi ; Chen, Hansen ; He, Yachong ; Fu, Shuping ; Liu, Haosheng ; Wang, Qi ; Shen, Jiangang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c418t-2869af2f69819ac197b2547a223f2d1ba4e2bac4d331b9de588c2af39eaa59ab3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>14-3-3 protein</topic><topic>AKT protein</topic><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Caveolin-1</topic><topic>Cell Biology</topic><topic>Cell differentiation</topic><topic>Cell proliferation</topic><topic>Cyclin D1</topic><topic>Epidermal growth factor receptors</topic><topic>Gel electrophoresis</topic><topic>Ischemia</topic><topic>Janus kinase 2</topic><topic>Learning</topic><topic>Neural stem cells</topic><topic>Neurobiology</topic><topic>Neurogenesis</topic><topic>Neurological diseases</topic><topic>Neurology</topic><topic>Neuroprotection</topic><topic>Neurosciences</topic><topic>Original Article</topic><topic>Proteomics</topic><topic>Recovery of function</topic><topic>Signal transduction</topic><topic>Stat3 protein</topic><topic>Stem cell transplantation</topic><topic>Stem cells</topic><topic>Stroke</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Xi</creatorcontrib><creatorcontrib>Chen, Hansen</creatorcontrib><creatorcontrib>He, Yachong</creatorcontrib><creatorcontrib>Fu, Shuping</creatorcontrib><creatorcontrib>Liu, Haosheng</creatorcontrib><creatorcontrib>Wang, Qi</creatorcontrib><creatorcontrib>Shen, Jiangang</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central 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Jak2/Stat3/Cyclin D1 Signaling Cascades</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><date>2020-10-01</date><risdate>2020</risdate><volume>57</volume><issue>10</issue><spage>4305</spage><epage>4321</epage><pages>4305-4321</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Buyang Huanwu Decoction (BHD), a classic traditional Chinese medicine (TCM) formula, has been used for recovering neurological dysfunctions and treating post-stroke disability in China for 200 years. In the present study, we investigated the effects of BHD on inhibiting neuronal apoptosis, promoting proliferation and differentiation of neural stem cells (NSCs) and neurite formation and enhancing learning and memory functional recovery in an experimental rat ischemic stroke model. BHD significantly reduced infarct volume and decreased cell apoptosis in the ischemic brain. BHD enhanced neuronal cell viability in vitro. BHD dose-dependently promoted the proliferation of NSCs in ischemic rat brains in vivo. Moreover, BHD promoted neuronal and astrocyte differentiation in primary cultured NSCs in vitro. Water maze test revealed that BHD promoted the recovery of learning function but not memory functions in the transient ischemic rats. We then investigated the changes of the cellular signaling molecules by using two-dimension (2D) gel electrophoresis and focused on the PI3K/Akt/Bad and Jak2/Stat3/cyclin D1signaling pathway to uncover its underlying mechanisms for its neuroprotective and neurogenetic effects. BHD significantly upregulated the expression of p-PI3K, p-Akt, and p-Bad as well as the expression of p-Jak, p-Stat3, and cyclin D1 in vitro and in vivo. In addition, BHD upregulated Hes1 and downregulated cav-1
in vitro
and in vivo. Taken together, these results suggest that BHD has neuroprotective effects and neurogenesis-promoting effects via activating PI3K/Akt/Bad and Jak2/Stat3/Cyclin D1 signaling pathways.
Graphical Abstract
Buyang Huanwu Decoction (BHD) activates the PI3K-AKT-BAD pathway in the ischemic brain for neuroprotection. BHD also activates JAK2/STAT3/Cyclin D1 signaling cascades for promoting neurogenesis in the hippocampus of post-ischemic brains. Moreover, BHD inhibits the expression of caveolin-1 and increases the expression of HES1 for promoting neuronal differentiation. The neuroprotective and neurogenesis-promoting effects in the hippocampus of post-ischemic brains promote learning ability.</abstract><cop>New York</cop><pub>Springer US</pub><doi>10.1007/s12035-020-02016-y</doi><tpages>17</tpages><orcidid>https://orcid.org/0000-0002-4199-8095</orcidid></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase 14-3-3 protein AKT protein Apoptosis Biomedical and Life Sciences Biomedicine Caveolin-1 Cell Biology Cell differentiation Cell proliferation Cyclin D1 Epidermal growth factor receptors Gel electrophoresis Ischemia Janus kinase 2 Learning Neural stem cells Neurobiology Neurogenesis Neurological diseases Neurology Neuroprotection Neurosciences Original Article Proteomics Recovery of function Signal transduction Stat3 protein Stem cell transplantation Stem cells Stroke |
| title | Proteomics-Guided Study on Buyang Huanwu Decoction for Its Neuroprotective and Neurogenic Mechanisms for Transient Ischemic Stroke: Involvements of EGFR/PI3K/Akt/Bad/14-3-3 and Jak2/Stat3/Cyclin D1 Signaling Cascades |
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