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Cerebral Ischemia Transient
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1. Attenuation of brain inflammatory response after focal cerebral ischemia/reperfusion with Xuesaitong injection in rats.
Match Strength: 14.885

OBJECTIVE: To investigate the neuro-protective effect of Xuesaitong Injection (XST) on brain inflammatory response after transient focal cerebral ischemia/reperfusion in rats. METHODS: Focal cerebral ischemia/reperfusion models of male rats were induced by transient occlusion for 2 h of middle cerebral artery (MCA) which was followed by 24 h reperfusion. XST was administered through intraperitoneal injection of 25 mg/kg or 50 mg/kg at 4 h after the onset of ischemia. After reperfusion for 24 h, the neurological function score was evaluated, the brain edema was detected with dry-wet weight ... Read More »
» Published in Chin J Integr Med. 2006 Sep;12(3):203-6.

2. Signal transducers and activators of transcription 5 contributes to erythropoietin-mediated neuroprotection against hippocampal neuronal death after transient global cerebral ischemia.
Match Strength: 13.136

The signal transducers and activators of transcription (STAT) proteins are a group of transcriptional factors. Among them, STAT5 initiates a pro-survival signaling cascade. So far, little has been known about the role of STAT5 in cerebral ischemia and reperfusion. This study examines the phosphorylation status of STAT5 in hippocampal CA1 in the early stage after transient global cerebral ischemia in rats. Our data show that the phosphorylation of STAT5 was increased in hippocampal CA1 at 1h and 3h ischemia. Taking advantage of the neuroprotective effect of erythropoietin (EPO) in CA1, we ... Read More »
» Published in Neurobiol Dis. 2007 Jan;25(1):45-53. Epub 2006 Sep 27.

3. Altered PPARgamma expression and activation after transient focal ischemia in rats.
Match Strength: 10.437

Stroke is a devastating disease with limited treatment options. Recently, we found that the peroxisome proliferator-activated receptor-gamma (PPARgamma) agonists troglitazone and pioglitazone reduce injury and inflammation in a rat model of transient cerebral ischemia. The mechanism of this protection is unclear, as these agents can act through PPAR-gamma activation or through PPAR-gamma-independent mechanisms. Therefore, we examined PPAR-gamma expression, DNA binding and transcriptional activity following stroke. In addition, we used a PPAR-gamma antagonist, T0070907, to determine the role of ... Read More »
» Published in Eur J Neurosci. 2006 Sep;24(6):1653-63.

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