Dutch
Albanian
Arabic
Armenian
Azerbaijani
Belarusian
Bengali
Bosnian
Catalan
Czech
Danish
Deutsch
Dutch
English
Estonian
Finnish
Français
Greek
Haitian Creole
Hebrew
Hindi
Hungarian
Icelandic
Indonesian
Irish
Italian
Japanese
Korean
Latvian
Lithuanian
Macedonian
Mongolian
Norwegian
Persian
Polish
Portuguese
Romanian
Russian
Serbian
Slovak
Slovenian
Spanish
Swahili
Swedish
Turkish
Ukrainian
Vietnamese
Български
中文(简体)
中文(繁體)
Neuroscience 2017-May

Combined metabolic and transcriptional profiling identifies pentose phosphate pathway activation by HSP27 phosphorylation during cerebral ischemia.

Alleen geregistreerde gebruikers kunnen artikelen vertalen
Log in Schrijf in
De link wordt op het klembord opgeslagen
Taichiro Imahori
Kohkichi Hosoda
Tomoaki Nakai
Yusuke Yamamoto
Yasuhiro Irino
Masakazu Shinohara
Naoko Sato
Takashi Sasayama
Kazuhiro Tanaka
Hiroaki Nagashima

Sleutelwoorden

Abstract

The metabolic pathophysiology underlying ischemic stroke remains poorly understood. To gain insight into these mechanisms, we performed a comparative metabolic and transcriptional analysis of the effects of cerebral ischemia on the metabolism of the cerebral cortex using middle cerebral artery occlusion (MCAO) rat model. Metabolic profiling by gas-chromatography/mass-spectrometry analysis showed clear separation between the ischemia and control group. The decreases of fructose 6-phosphate and ribulose 5-phosphate suggested enhancement of the pentose phosphate pathway (PPP) during cerebral ischemia (120-min MCAO) without reperfusion. Transcriptional profiling by microarray hybridization indicated that the Toll-like receptor and mitogen-activated protein kinase (MAPK) signaling pathways were upregulated during cerebral ischemia without reperfusion. In relation to the PPP, upregulation of heat shock protein 27 (HSP27) was observed in the MAPK signaling pathway and was confirmed through real-time polymerase chain reaction. Immunoblotting showed a slight increase in HSP27 protein expression and a marked increase in HSP27 phosphorylation at serine 85 after 60-min and 120-min MCAO without reperfusion. Corresponding upregulation of glucose 6-phosphate dehydrogenase (G6PD) activity and an increase in the NADPH/NAD+ ratio were also observed after 120-min MCAO. Furthermore, intracerebroventricular injection of ataxia telangiectasia mutated (ATM) kinase inhibitor (KU-55933) significantly reduced HSP27 phosphorylation and G6PD upregulation after MCAO, but that of protein kinase D inhibitor (CID755673) did not affect HSP27 phosphorylation. Consequently, G6PD activation via ischemia-induced HSP27 phosphorylation by ATM kinase may be part of an endogenous antioxidant defense neuroprotection mechanism during the earliest stages of ischemia. These findings have important therapeutic implications for the treatment of stroke.

Word lid van onze
facebookpagina

De meest complete database met geneeskrachtige kruiden, ondersteund door de wetenschap

  • Werkt in 55 talen
  • Kruidengeneesmiddelen gesteund door de wetenschap
  • Kruidenherkenning door beeld
  • Interactieve GPS-kaart - tag kruiden op locatie (binnenkort beschikbaar)
  • Lees wetenschappelijke publicaties met betrekking tot uw zoekopdracht
  • Zoek medicinale kruiden op hun effecten
  • Organiseer uw interesses en blijf op de hoogte van nieuwsonderzoek, klinische onderzoeken en patenten

Typ een symptoom of een ziekte en lees over kruiden die kunnen helpen, typ een kruid en zie ziekten en symptomen waartegen het wordt gebruikt.
* Alle informatie is gebaseerd op gepubliceerd wetenschappelijk onderzoek

Google Play badgeApp Store badge