Adipokinetic hormone exerts its anti-oxidative effects using a conserved signal-transduction mechanism involving both PKC and cAMP by mobilizing extra- and intracellular Ca2+ stores.
作者： Andrea Bednářová , Dalibor Kodrík , Natraj Krishnan
DOI: 10.1016/J.CBPC.2013.07.002
关键词: Thapsigargin 、 Cyclic adenosine monophosphate 、 Forskolin 、 Biology 、 Protein kinase A 、 Protein kinase C 、 Signal transduction 、 Activator (genetics) 、 Adipokinetic hormone 、 Internal medicine 、 Endocrinology
摘要: Abstract The involvement of members the adipokinetic hormone (AKH) family in regulation response to oxidative stress (OS) has been reported recently. However, despite these neuropeptides being best studied insect hormones, their precise signaling pathways OS responsive role remain be elucidated. In this study, we have used an vitro assay determine importance extra and intra-cellular Ca2 + stores as well protein kinase C (PKC) cyclic adenosine 3′,5′-monophosphate (cAMP) by which AKH exerts its anti-oxidative effects. Lipid peroxidation product (4-HNE) was significantly enhanced membrane fluidity reduced microsomal fractions isolated brains (CNS) Pyrrhocoris apterus when treated with hydrogen peroxide (H2O2), whereas biomarkers were control levels H2O2 co-treated Pyrap-AKH. effects mitigation CNS negated treatments conducted presence channel inhibitors (CdCl2 thapsigargin). Presence either bisindolylmaliemide or chelyrythrine chloride (inhibitors PKC) incubating medium also compromised function AKH. supplementing phorbol myristate acetate (PMA, activator forskolin (an cAMP) restored protective exogenous treatment reducing 4-HNE increasing levels. Taken together, our results strongly implicate both PKC cAMP AKHs' action mobilizing Ca2 +.
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