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Activation of STAT3 induced by cerebral ischemia in rat hippoca mpus and its possible mechanisms

LI Hong Chun

Research Centere of Biochenastry and Molecular Biology，Xuzhou Medical College，Xuzhou 221002

Abstract

It has been demonstrated that signal transducer and activator of transcriptiorr3(STAT3) is activated after cerebral isthe mia/ reperfusion(I/助in cortex and striatum .In this study ,we investigated whether STAT3 was rapidly activated in hippocampus by cerebral ischemia without reperfusion in four-vessel occlusion(4- VO) model of Sprague- Dawley(SD) rats.The results showed that tyrosine phosphorylation and DNA binding activity of STAT3 was rapidly increased by ischemia.The p-STAT3 level in cytoplasmincreased 5 min after occlusion and reached a peak at 10 min following ischemia(1.7 fol ds二sham) by means of immunoblotting (113).P STAT3 in nucleus was gradually enhanced with its peak activity occurring at 30 min of ischemia(2. 3 folds二sham).Electrophoretic mobility shift assay(EMSA) with STAT3 probe demonstrated that DNA binding activity of STAT3 in nuclear extracts increased from 5 min and peaked at 30 min of ischemia(3. 2 folds二sham).These changes were prevented by genistein(a protein tyrosine kinase inhibitor) and antioxidant N acetyl- L- cysteine(NA()，but promoted by sodium orthovanadate(a protein phosphatase inhibitor)，which were administered to the SD rats 20 min before ischemia.These results indicate that the activation of STAT3 following cerebral ischemia may be modulated by PTK/ PTP，and that this pathway may be of benefit to the adaptation of the hippocampal neurons to oxidative stress.

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Citing This Article：

LI Hong Chun. Activation of STAT3 induced by cerebral ischemia in rat hippoca mpus and its possible mechanisms. Acta Physiol Sin 2003; 55 (3): (in Chinese with English abstract).