JNK inhibition and inflammation after cerebral ischemia

Abstract The c-Jun-N-terminal kinase signaling pathway (JNK) is highly activated during ischemia and plays an important role in apoptosis and inflammation. We have previously demonstrated that D-JNKI1, a specific JNK inhibitor, is strongly neuroprotective in animal models of stroke. We presently eva...

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Veröffentlicht in:	Brain, behavior, and immunity behavior, and immunity, 2010-07, Vol.24 (5), p.800-811
Hauptverfasser:	Benakis, Corinne, Bonny, Christophe, Hirt, Lorenz
Format:	Artikel
Sprache:	eng
Schlagworte:	Allergy and Immunology Animals Brain Ischemia - metabolism Brain Ischemia - pathology c-Jun-N-terminal kinase Hippocampus - drug effects Hippocampus - metabolism Hippocampus - pathology Immunohistochemistry Inflammation Inflammation - metabolism Inflammation - pathology JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors JNK Mitogen-Activated Protein Kinases - metabolism Male Mice Microglia Microglia - drug effects Microglia - metabolism Microglia - pathology Middle cerebral artery occlusion Neurons - drug effects Neurons - metabolism Neurons - pathology Neuroprotection Organ Culture Techniques Oxygen and glucose deprivation Peptides - pharmacology Phosphorylation - drug effects Psychiatry Rats Rats, Sprague-Dawley
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