期刊
EUROPEAN JOURNAL OF PHARMACOLOGY
卷 535, 期 1-3, 页码 114-124出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2006.01.037
关键词
cerebral ischemia; hippocampus; hepatocyte growth factor; extracellular signal-regulated kinase
Hepatocyte growth factor (HGF) has been implicated in protection against several types of cell injuries. We investigated the effects of human recombinant HGF (hrHGF) on the selective neuronal cell death in the hippocampal CA1 region after transient forebrain ischemia in rats and explored the nature of the intracellular signaling pathway for the protection against this neuronal injury. hrHGF was injected continuously into the hippocampal CA1 region directly using an osmotic pump from 10 min to 72 h after the start of reperfusion. The marked increase in the number of TUNEL-positive cells found in the CA1 region after ischernia was almost completely abolished by the hrHGF treatment. Akt phosphorylation as well as IKB phosphorylation, which has been implicated in events downstream of the Akt, was not affected by hrHGF treatment. Extracellular signal-regulated kinase (ERK) phosphorylation was decreased in the CA1 region with time after ischernia. hrHGF increased or recovered ERK phosphorylation without changing the total amount of ERK protein. Immunohistochemical analysis demonstrated that phosphorylated ERK was colocalized with a neuronal nucleus marker NeuN in the hippocampal CA1 region of ischemic rats with hrHGF treatment at the early period after reperfusion. These results suggest that the protective effects of hrHGF against neuronal death in the hippocampal CA1 after transient forebrain ischernia could be related to an ERK-dependent pathway. (c) 2006 Elsevier B.V. All rights reserved.
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