[Expression of FAS and FASL genes in brain and effect of flunarizine on these expressions in rats after global ischemia-reperfusion]

Yao Xue Xue Bao. 2000 Nov;35(11):810-3.
[Article in Chinese]

Abstract

Aim: 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.

Conclusion: 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.

MeSH terms

  • Animals
  • Apoptosis
  • Brain / metabolism
  • Brain Ischemia / genetics*
  • Brain Ischemia / pathology
  • Calcium Channel Blockers / pharmacology*
  • Fas Ligand Protein
  • Flunarizine / pharmacology*
  • Male
  • Membrane Glycoproteins / genetics*
  • Rats
  • Rats, Wistar
  • Reperfusion Injury / genetics*
  • Reperfusion Injury / pathology
  • fas Receptor / genetics*

Substances

  • Calcium Channel Blockers
  • Fas Ligand Protein
  • Faslg protein, rat
  • Membrane Glycoproteins
  • fas Receptor
  • Flunarizine