NG-nitro-L-arginine methyl ester reduces necrotic but not apoptotic cell death induced by reversible focal ischemia in rat.
During cerebral ischemia, nitric oxide (NO) production via stimulation of NO synthase, is likely one of the major events leading to neuronal death. Recently, we have demonstrated that after reversible focal ischemia, apoptosis was implicated in the penumbra whereas necrosis was prominent in the ischemic core. We have now examined the effect of a non-specific inhibitor of NO synthase, NG-nitro-L-arginine methyl ester (L-NAME, 3 ing kg-1 i.p., 5 min and 3 h after the onset of ischemia), on the progress of apoptotic and necrotic nuclei following transient focal cerebral ischemia, using DNA electrophoresis and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick-end labeling (TUNEL assay). Our results indicated that L-NAME prevented the loss of necrotic, but not apoptotic cells.
Charriaut-Marlangue
C
C
Université R. Descartes, INSERM U29, Paris, France.
Margaill
I
I
Borrega
F
F
Plotkine
M
M
Ben-Ari
Y
Y
D000818:Animals; D017209:Apoptosis; D002545:Brain Ischemia / Q000473:pathology / Q000517:prevention & control*; D053938:DNA Fragmentation / Q000187:drug effects; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology*; D009336:Necrosis; D051381:Rats; D017207:Rats, Sprague-Dawley
D019331:NG-Nitroarginine Methyl Ester