Exogenous adenosine enhances caspase-3 activity in warm renal ischaemia.
Renal injury due to ischaemia/reperfusion (I/R) leads to impaired renal function. One of the essential pathological changes thereby is cell death due to apoptosis. This study investigated the effect of adenosine administration on caspase-3 (C3) activity and expression during warm renal ischaemia in rat kidney and the role of nitric oxide (NO) as a mediator of the adenosine-induced effect. The following experimental groups were studied: control, ischaemia, ischaemia with adenosine administration, ischaemia with adenosine and N-nitro- l-arginine methyl ester (L-NAME) treatment and ischaemia with NO donor administration. C3 activity was measured and its protein expression determined by Western blot analysis. Supplementation of adenosine or NO during ischaemia increased C3 activity and protein expression but the effect of adenosine was reversed in rats treated with L-NAME. We conclude that adenosine increases C3 activity through an NO-dependent mechanism.
Sola
A
A
Department of Experimental Pathology, Instituto de Investigaciones Biomédicas de Barcelona, C/Rosselló 161, 7 feminine planta, 08036 Barcelona, Spain.
Alfaro
V
V
Viñas
J L
JL
Hotter
G
G
D000241:Adenosine / Q000494:pharmacology*; D000818:Animals; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000378:metabolism; D020287:In Situ Nick-End Labeling; D007511:Ischemia / Q000378:metabolism* / Q000473:pathology; D007668:Kidney / Q000098:blood supply* / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D020030:Nitric Oxide Donors / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury
D004791:Enzyme Inhibitors; D020030:Nitric Oxide Donors; D009569:Nitric Oxide; C505410:Casp3 protein, rat; D053148:Caspase 3; D020169:Caspases; D000241:Adenosine; D019331:NG-Nitroarginine Methyl Ester