[Expression of FAS and FASL genes in brain and effect of flunarizine on these expressions in rats after global ischemia-reperfusion].
OBJECTIVE
To explore the expression of Fas and FasL genes after ischemia-reperfusion in rats and the effect of flunarizine.


METHODS
Ischemia was induced by four-vessel occlusion for 30 min following reperfusion in rats. The biopsy tissues from brain were immunohistochemically assayed with Fas and FasL genes polyclonal antibody.


RESULTS
The expression of Fas was increased as early as 6 h after the onset of reperfusion. The peak of the expression of Fas occurred 24-48 h after ischemia-reperfusion. The expression of FasL was observed 12 h after ischemia-reperfusion and peaked at 48-72 h. The expression of Fas and FasL gene was quite obvious in the cortex and hippocampus CA1, the more sensitive areas to ischemic injury. Flunarizine i.p. 10 mg.kg-1 and 20 mg.kg-1 obviously inhibited the expression of Fas and FasL in dose-dependent manner.


CONCLUSIONS
Expression of Fas and FasL in cerebral cortex and hippocampus can be induced by global ischemia-reperfusion. Flunarizine significantly inhibited the expression of Fas and FasL genes following ischemia-reperfusion.
Liu
Y J
YJ
Department of Pharmacology, Chongqing University of Medical Sciences, Chongqing 400016, China.
Xue
C S
CS
Zhou
Q X
QX
D000818:Animals; D017209:Apoptosis; D001921:Brain / Q000378:metabolism; D002545:Brain Ischemia / Q000235:genetics* / Q000473:pathology; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D053222:Fas Ligand Protein; D005444:Flunarizine / Q000494:pharmacology*; D008297:Male; D008562:Membrane Glycoproteins / Q000235:genetics*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000235:genetics* / Q000473:pathology; D019014:fas Receptor / Q000235:genetics*
D002121:Calcium Channel Blockers; D053222:Fas Ligand Protein; C505662:Faslg protein, rat; D008562:Membrane Glycoproteins; D019014:fas Receptor; D005444:Flunarizine