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BHDPC Is a Novel Neuroprotectant That Provides Anti-neuroinflammatory and
Neuroprotective Effects by Inactivating NF-?B and Activating PKA/CREB
#MMPMID29988625
Li C
; Chen T
; Zhou H
; Feng Y
; Hoi MPM
; Ma D
; Zhao C
; Zheng Y
; Lee SMY
Front Pharmacol
2018[]; 9
(?): 614
PMID29988625
show ga
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-?B) via interfering with the degradation of the inhibitor of
kappa B (I?B) and phosphorylation of I?B, the I?B 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.
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