Leptomycin B attenuates neuronal death via PKA- and PP2B-mediated ERK1/2 activation in the rat hippocampus following status epilepticus.
作者： Su-Ji Min , Hye-Won Hyun , Tae-Cheon Kang
DOI: 10.1016/J.BRAINRES.2017.06.002
关键词: Biochemistry 、 Chemistry 、 Pilocarpine 、 H-89 、 Phosphorylation 、 Status epilepticus 、 Cyclosporin a 、 Kinase 、 Pharmacology 、 Neuroprotection 、 Protein kinase A
摘要: Abstract Leptomycin B (LMB), originally developed as an anti-fungal agent, has potent neuroprotective properties against status epilepticus (SE, a prolonged seizure activity). However, the pharmacological profiles and mechanisms of LMB for neuroprotection remain elusive. In present study, we found that increased phosphorylation levels protein kinase A (PKA) catalytic subunits, phosphatase 2B (PP2B, calcineurin) extracellular signal–regulated 1/2 (ERK1/2) under normal condition, abolished SE-induced neuronal death. Co-treatment H-89 (a PKA inhibitor) with could not affect latency its severity in response to pilocarpine. co-treatment abrogated protective effect on damage. Cyclosporin (CsA, PP2B effectively prevented death without altered susceptibility pilocarpine more than alone. inhibited LMB-mediated ERK1/2 phosphorylation, but CsA enhanced it. U0126 (an alterations phosphorylations. To best our knowledge, data demonstrate previously unreported potential role SE via PKA- PP2B-mediated activation.
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