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Updated: Jan 27, 2026

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets
Published on: November 22, 2024
Down-regulation of platelet-activating factor receptor gene expression during focal reversible cerebral ischemia in
Xiong Zhang1, Xi-Long Pan, Xin-Tong Liu
1Department of Neurology, Guangdong Provincial People's Hospital, Nanfang Medical University, 106, Zhongshan Er Road, Guangzhou, Guangdong Province 510080, PR China.
Abstract:
Platelet-activating factor (PAF) is an endogenous potent phospholipid mediator in stroke and related to the post-ischemic brain damage. The aim of this study was to investigate the regulation and mechanisms of PAF receptor gene expression in the perifocal regions of cerebral infarction after middle cerebral artery occlusion/reperfusion. Sixty mature Wistar rats were randomly divided into 12 groups: sham-operated control group, simple ischemia 90 min group, 6, 12, 18 h, 1 day (1 d), 2, 3, 4, 5, 6, 7 d reperfusion groups. After the right middle cerebral artery occluded, the rats were suffered from ischemia for 90 min, and then reperfusion was allowed for different time courses. Reverse transcription-polymerase chain reaction (RT-PCR) and radioimmunoassay were applied to evaluate the PAF receptor messenger RNA (mRNA) expression and PAF levels in the perifocal regions of cerebral infarction respectively. RT-PCR analysis revealed that PAF receptor mRNA was 0.95 +/- 0.15 in control group. However, following ischemia-reperfusion, the levels of PAF receptor mRNA progressively decreased until 2 d of reperfusion (0.54 +/- 0.10), then returned to control group's levels gradually. Compared with the control group's (582 +/- 72 pg/g wet weight), the PAF concentrations of simple ischemic and 6, 12, 18 h, 1, 2 d reperfusion group were significantly higher than that of any other groups. These results indicate that PAF receptor gene expression may be subject to down-regulation in the perifocal regions of cerebral infarction after cerebral ischemia-reperfusion and relative to the increase of endogenous PAF concentrations.
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