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Caffeic acid phenethyl amide ameliorates ischemia/reperfusion injury and cardiac dysfunction in streptozotocin-induced diabetic rats.

AbstractBACKGROUND:
Caffeic acid phenethyl ester (CAPE) has been shown to protect the heart against ischemia/reperfusion (I/R) injury by various mechanisms including its antioxidant effect. In this study, we evaluated the protective effects of a CAPE analog with more structural stability in plasma, caffeic acid phenethyl amide (CAPA), on I/R injury in streptozotocin (STZ)-induced type 1 diabetic rats.
METHODS:
Type 1 diabetes mellitus was induced in Sprague-Dawley rats by a single intravenous injection of 60 mg/kg STZ. To produce the I/R injury, the left anterior descending coronary artery was occluded for 45 minutes, followed by 2 hours of reperfusion. CAPA was pretreated intraperitoneally 30 minutes before reperfusion. An analog devoid of the antioxidant property of CAPA, dimethoxyl CAPA (dmCAPA), and a nitric oxide synthase (NOS) inhibitor (Nω-nitro-l-arginine methyl ester [l-NAME]) were used to evaluate the mechanism involved in the reduction of the infarct size following CAPA-treatment. Finally, the cardioprotective effect of chronic treatment of CAPA was analyzed in diabetic rats.
RESULTS:
Compared to the control group, CAPA administration (3 and 15 mg/kg) significantly reduced the myocardial infarct size after I/R, while dmCAPA (15 mg/kg) had no cardioprotective effect. Interestingly, pretreatment with a NOS inhibitor, (L-NAME, 3 mg/kg) eliminated the effect of CAPA on myocardial infarction. Additionally, a 4-week CAPA treatment (1 mg/kg, orally, once daily) started 4 weeks after STZ-induction could effectively decrease the infarct size and ameliorate the cardiac dysfunction by pressure-volume loop analysis in STZ-induced diabetic animals.
CONCLUSIONS:
CAPA, which is structurally similar to CAPE, exerts cardioprotective activity in I/R injury through its antioxidant property and by preserving nitric oxide levels. On the other hand, chronic CAPA treatment could also ameliorate cardiac dysfunction in diabetic animals.
AuthorsYi-Jin Ho, An-Sheng Lee, Wen-Pin Chen, Wei-Lung Chang, Ying-Kang Tsai, Hsi-Lin Chiu, Yueh-Hsiung Kuo, Ming-Jai Su
JournalCardiovascular diabetology (Cardiovasc Diabetol) Vol. 13 Pg. 98 (Jun 12 2014) ISSN: 1475-2840 [Electronic] England
PMID24923878 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Caffeic Acids
  • Hypoglycemic Agents
  • caffeic acid phenethyl amide
Topics
  • Animals
  • Caffeic Acids (therapeutic use)
  • Diabetes Mellitus, Experimental (drug therapy, pathology)
  • Hypoglycemic Agents (therapeutic use)
  • Male
  • Myocardial Infarction (pathology, prevention & control)
  • Myocardial Reperfusion Injury (pathology, prevention & control)
  • Rats
  • Rats, Sprague-Dawley

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