BHDPC Is a Novel Neuroprotectant That Provides Anti-neuroinflammatory and Neuroprotective Effects by Inactivating NF-κB and Activating PKA/CREB.
cam.issuedOnline | 2018-06-25 | |
dc.contributor.author | Li, Chuwen | |
dc.contributor.author | Chen, Tongkai | |
dc.contributor.author | Zhou, Hefeng | |
dc.contributor.author | Feng, Yu | |
dc.contributor.author | Hoi, Maggie PM | |
dc.contributor.author | Ma, Dan | |
dc.contributor.author | Zhao, Chao | |
dc.contributor.author | Zheng, Ying | |
dc.contributor.author | Lee, Simon MY | |
dc.contributor.orcid | Zhao, Chao [0000-0003-1144-1621] | |
dc.date.accessioned | 2018-10-03T04:44:12Z | |
dc.date.available | 2018-10-03T04:44:12Z | |
dc.date.issued | 2018 | |
dc.description.abstract | Microglia-mediated neuroinflammatory responses are inevitable and important pathological processes in several kinds of disorder of the central nervous system (CNS). Therefore, alleviating activated microglia-induced inflammatory process might be a valuable therapeutic approach to neuroinflammation-related diseases. In the present study, we investigated BHDPC, a novel neuroprotectant discovered in our previous study that had anti-inflammatory effects under neuroinflammatory conditions. First, we found that BHDPC could inhibit neuroinflammatory responses and promote microglial M2 phenotype polarization in both lipopolysaccharide (LPS)-activated BV-2 microglia l cells. Furthermore, BHDPC provided protective actions against neuroinflammation-induced neurotoxicity in HT22 mouse hippocampal cells co-cultured with activated BV-2 microglia. Further experiments demonstrated that BHDPC could suppress LPS-induced activation of transcription factor nuclear factor kappa B (NF-κB) via interfering with the degradation of the inhibitor of kappa B (IκB) and phosphorylation of IκB, the IκB kinase (IKK). Moreover, we also found that BHDPC could induce phosphorylation of cAMP-dependent protein kinase A (PKA) and cAMP-response element-binding protein (CREB) in BV-2 microglial cells. Also, using the PKA-specific inhibitor, we found that BHDPC-induced CREB phosphorylation was dependent on PKA, which also contributed to BHDPC-mediated anti-inflammation and neuroprotection. | |
dc.format.medium | Electronic-eCollection | |
dc.identifier.doi | 10.17863/CAM.30413 | |
dc.identifier.eissn | 1663-9812 | |
dc.identifier.issn | 1663-9812 | |
dc.identifier.uri | https://www.repository.cam.ac.uk/handle/1810/283050 | |
dc.language | eng | |
dc.language.iso | eng | |
dc.publisher | Frontiers Media SA | |
dc.publisher.url | http://dx.doi.org/10.3389/fphar.2018.00614 | |
dc.rights | Attribution 4.0 International | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | |
dc.subject | BHDPC | |
dc.subject | CREB | |
dc.subject | NF-κB | |
dc.subject | PKA | |
dc.subject | microglia | |
dc.subject | neuroinflammation | |
dc.title | BHDPC Is a Novel Neuroprotectant That Provides Anti-neuroinflammatory and Neuroprotective Effects by Inactivating NF-κB and Activating PKA/CREB. | |
dc.type | Article | |
dcterms.dateAccepted | 2018-05-22 | |
prism.publicationDate | 2018 | |
prism.publicationName | Front Pharmacol | |
prism.startingPage | 614 | |
prism.volume | 9 | |
rioxxterms.licenseref.startdate | 2018-01 | |
rioxxterms.licenseref.uri | http://www.rioxx.net/licenses/all-rights-reserved | |
rioxxterms.type | Journal Article/Review | |
rioxxterms.version | VoR | |
rioxxterms.versionofrecord | 10.3389/fphar.2018.00614 |
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