title: Protective effects of p-nitro caffeic acid phenethyl ester on acute myocardial ischemia-reperfusion injury in rats.
abstract: Myocardial ischemia-reperfusion (IR) causes widespread cardiomyocyte dysfunction, including apoptosis and necrosis. The present study aimed to investigate the possible cardioprotective effects of p-nitro caffeic acid phenethyl ester (CAPE-NO2) on myocardial IR-induced injuryin vivo. To generate a rat model of myocardial IR, the left anterior descending coronary artery was occluded for 30 min, followed by reperfusion for 2 h. The rats were administered either the sham treatment (the sham and IR control groups) or the therapeutic agents [the caffeic acid phenethyl ester (CAPE) and CAPE-NO2groups] 10 min prior to the occlusion. Myocardial IR-induced injury is characterized by: A significant increase in the levels of myocardial enzymes, including creatine kinase, lactate dehydrogenase and aspartate transaminase; a marked increase in intercellular adhesion molecule 1 expression levels, lipid peroxidation products and inflammatory mediators; and a significant decrease in myocardial antioxidants, including catalase, total superoxide dismutase and glutathione peroxidase. In the present study, pretreatment with CAPE-NO2significantly ameliorated these changes, and decreased the infarct size, as compared with the IR control group (10.32±3.8 vs. 35.65±5.4%). Furthermore, western blotting demonstrated that pretreatment with CAPE-NO2downregulated the myocardial IR-induced protein expression levels of B-cell lymphoma-2 (Bcl-2)-associated X protein (Bax), cleaved caspase-3, P38 and the Bax/Bcl-2 ratio. CAPE-NO2also upregulated the myocardial IR-induced expression levels of Bcl-2, phosphoinositide-3-kinase, phosphorylated Akt and mammalian target of rapamycin. In conclusion, the results of the present study indicated that CAPE-NO2demonstrated improved cardioprotective effects, as compared with CAPE; therefore, CAPE-NO2may represent a novel approach to pharmacological cardioprotection.
authors.affiliation: College of Pharmaceutical Sciences and Chinese Medicine, Southwest University, Chongqing 400716, P.R. China.
authors.forename: Qin
authors.initials: Q
authors.lastname: DU
authors.affiliation: College of Pharmaceutical Sciences and Chinese Medicine, Southwest University, Chongqing 400716, P.R. China.
authors.forename: Chunzhi
authors.initials: C
authors.lastname: Hao
authors.affiliation: College of Pharmaceutical Sciences and Chinese Medicine, Southwest University, Chongqing 400716, P.R. China.
authors.forename: Jing
authors.initials: J
authors.lastname: Gou
authors.affiliation: College of Pharmaceutical Sciences and Chinese Medicine, Southwest University, Chongqing 400716, P.R. China.
authors.forename: Xiaoli
authors.initials: X
authors.lastname: Li
authors.affiliation: College of Pharmaceutical Sciences and Chinese Medicine, Southwest University, Chongqing 400716, P.R. China.
authors.forename: Kaili
authors.initials: K
authors.lastname: Zou
authors.affiliation: College of Pharmaceutical Sciences and Chinese Medicine, Southwest University, Chongqing 400716, P.R. China.
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: He
authors.affiliation: College of Pharmaceutical Sciences and Chinese Medicine, Southwest University, Chongqing 400716, P.R. China.
authors.forename: Zhubo
authors.initials: Z
authors.lastname: Li
keywords: caffeic acid phenethyl ester; derivative; inflammation; oxidative stress; phosphoinositide-3-kinase/Akt/mammalian target of rapamycin signaling pathway