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- Publisher Website: 10.1007/s12035-020-02016-y
- Scopus: eid_2-s2.0-85088458202
- PMID: 32700252
- WOS: WOS:000551397100001
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Article: 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 | 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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Authors | |
Keywords | Buyang Huanwu Decoction Stroke Neurogenesis Neuroprotection |
Issue Date | 2020 |
Publisher | Springer. The Journal's web site is located at https://www.springer.com/biomed/neuroscience/journal/12035 |
Citation | Molecular Neurobiology, 2020, v. 57, p. 4305-4321 How to Cite? |
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. |
Persistent Identifier | http://hdl.handle.net/10722/293710 |
ISSN | 2023 Impact Factor: 4.6 2023 SCImago Journal Rankings: 1.339 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Chen, X | - |
dc.contributor.author | Chen, H | - |
dc.contributor.author | HE, Y | - |
dc.contributor.author | Fu, S | - |
dc.contributor.author | Liu, H | - |
dc.contributor.author | Wang, Q | - |
dc.contributor.author | Shen, J | - |
dc.date.accessioned | 2020-11-23T08:20:41Z | - |
dc.date.available | 2020-11-23T08:20:41Z | - |
dc.date.issued | 2020 | - |
dc.identifier.citation | Molecular Neurobiology, 2020, v. 57, p. 4305-4321 | - |
dc.identifier.issn | 0893-7648 | - |
dc.identifier.uri | http://hdl.handle.net/10722/293710 | - |
dc.description.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. | - |
dc.language | eng | - |
dc.publisher | Springer. The Journal's web site is located at https://www.springer.com/biomed/neuroscience/journal/12035 | - |
dc.relation.ispartof | Molecular Neurobiology | - |
dc.rights | Accepted Manuscript (AAM) This is a post-peer-review, pre-copyedit version of an article published in [insert journal title]. The final authenticated version is available online at: https://doi.org/[insert DOI] | - |
dc.subject | Buyang Huanwu Decoction | - |
dc.subject | Stroke | - |
dc.subject | Neurogenesis | - |
dc.subject | Neuroprotection | - |
dc.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 | - |
dc.type | Article | - |
dc.identifier.email | Shen, J: shenjg@hku.hk | - |
dc.identifier.authority | Shen, J=rp00487 | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1007/s12035-020-02016-y | - |
dc.identifier.pmid | 32700252 | - |
dc.identifier.scopus | eid_2-s2.0-85088458202 | - |
dc.identifier.hkuros | 319900 | - |
dc.identifier.volume | 57 | - |
dc.identifier.spage | 4305 | - |
dc.identifier.epage | 4321 | - |
dc.identifier.isi | WOS:000551397100001 | - |
dc.publisher.place | United States | - |