The effect of caffeic acid phenethyl ester on short-term acute myocardial ischemia.
BACKGROUND
We previously showed that caffeic acid phenethyl ester (CAPE) attenuated NO production, reduced apoptosis, diminished serum CK and AST activities, and is cardio-protective in rat heart subjected to ischemia/reperfusion (I/R). We now studied the short-term cardio-protective effect of CAPE in an I/R rat heart model.


METHODS
Wistar rats were divided into four groups: (i) sham-operated, (ii) I/R, (iii) I/R+CAPE, and (iv) I/R+glutathione. CAPE (10 micromol/kg) was infused i.v. 10 min before occlusion of the left anterior descending coronary artery (8 min) followed by reperfusion (8 min).


RESULTS
SOD (p < 0.010) and CAT (p < 0.014) activities were increased and GSH-Px (p < 0.019) activity decreased in the I/R group in cardiac tissues compared with the sham-operated group. There were no effects of CAPE on antioxidant enzyme activities after I/R. Glutathione administration led to decreased SOD activity (p < 0.024) and increased GSH-Px (p < 0.014) activity after I/R. The most prominent effects of CAPE were seen in XO and ADA activities, which were increased after I/R compared with the sham-operated group (p < 0.029 and p < 0.001, respectively). When CAPE was administered, XO and ADA activities were decreased compared with the I/R group (p < 0.045 and p < 0.001). ADA activity was also decreased in the I/R+glutathione group compared with the I/R group. No differences in basal heart rate or systolic or diastolic pressure were noted among the experimental groups.


CONCLUSIONS
This study demonstrates that CAPE exerts cardio-protective effects in short-term I/R of rat heart. This protective effect may be mediated by a combination of decreased XO activity and direct antioxidant effects.
Ince
Haluk
H
Istanbul University, Istanbul Medical Faculty, Department of Forensic Medicine, Istanbul, Turkey. hince@istanbul.edu.tr
Kandemir
Eyup
E
Bagci
Cahit
C
Gulec
Mukaddes
M
Akyol
Omer
O
D000208:Acute Disease; D000243:Adenosine Deaminase / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D002109:Caffeic Acids / Q000494:pharmacology*; D002316:Cardiotonic Agents / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D017202:Myocardial Ischemia / Q000188:drug therapy* / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy / Q000378:metabolism / Q000517:prevention & control; D009569:Nitric Oxide / Q000378:metabolism; D010626:Phenylethyl Alcohol / Q000031:analogs & derivatives* / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D014969:Xanthine Oxidase / Q000378:metabolism
D000975:Antioxidants; D002109:Caffeic Acids; D002316:Cardiotonic Agents; D009569:Nitric Oxide; D008315:Malondialdehyde; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D014969:Xanthine Oxidase; D000243:Adenosine Deaminase; C055494:caffeic acid phenethyl ester; D010626:Phenylethyl Alcohol