摘要
Background Peroxisome proliferator-activated receptor （PPAR） a is one of the subtypes of PPARs. It regulates metabolism of lipid and lipoprotein, as well as glucose homeostasis. In addition, PPARa influences cellular proliferation, inflammation, differentiation and apoptosis, which plays a vital role in cardiovascular diseases. The purpose of this study was to investigate the role and mechanisms of PPARa activation in relation to acute myocardial damage induced by isoproterenol in rats. Methods Thirty male Wister rats were randomly divided into control group, isoproterenol （Iso） injured group and fenofibrate （FF） treatment group. Acute myocardial damage caused by isoproterenol intraperitoneal injection induced ischemia was established. We determined the levels of creatine kinase （CK） and lactic dehydrogenase （LDH） in serum as well as the concentrations of free fatty acids （FFA） in serum and myocardium. The mRNA expressions of PPARa, muscular type carnitine palmitransferase （M-CPT-I） and medium chain lipid acetyl coenzyme A dehydrogenase （MCAD） were analyzed by reverse transcription-polymerase chain reaction （RT-PCR）. Results Compared with the control group, the levels of serum CK and LDH were significantly increased after FF and Iso treatments. Moreover, the concentrations of FFA in both serum and myocardium were obviously increased in the Iso group and FF group, while the mRNAexpressions of PPARa, M-CPT-I and MCAD declined, respectively （P〈0.01）. When compared with the Iso group, significant decreases in serum CK and LDH were observed in the FF group. The concentrations of FFA both in serum and myocardial tissue were markedly decreased in the FF group, while the expressions of PPARa, M-CPT-I and MCAD mRNA were increased （vs Iso, P〈0.01）. Conclusions The utilization of FFA was reduced in isoproterenol induced acute myocardial damage. PPARa activation by its activator fenofibrate may play a key role in energy metabolism in acute myocardial damage induced by isoproter
Background Peroxisome proliferator-activated receptor （PPAR） a is one of the subtypes of PPARs. It regulates metabolism of lipid and lipoprotein, as well as glucose homeostasis. In addition, PPARa influences cellular proliferation, inflammation, differentiation and apoptosis, which plays a vital role in cardiovascular diseases. The purpose of this study was to investigate the role and mechanisms of PPARa activation in relation to acute myocardial damage induced by isoproterenol in rats. Methods Thirty male Wister rats were randomly divided into control group, isoproterenol （Iso） injured group and fenofibrate （FF） treatment group. Acute myocardial damage caused by isoproterenol intraperitoneal injection induced ischemia was established. We determined the levels of creatine kinase （CK） and lactic dehydrogenase （LDH） in serum as well as the concentrations of free fatty acids （FFA） in serum and myocardium. The mRNA expressions of PPARa, muscular type carnitine palmitransferase （M-CPT-I） and medium chain lipid acetyl coenzyme A dehydrogenase （MCAD） were analyzed by reverse transcription-polymerase chain reaction （RT-PCR）. Results Compared with the control group, the levels of serum CK and LDH were significantly increased after FF and Iso treatments. Moreover, the concentrations of FFA in both serum and myocardium were obviously increased in the Iso group and FF group, while the mRNAexpressions of PPARa, M-CPT-I and MCAD declined, respectively （P〈0.01）. When compared with the Iso group, significant decreases in serum CK and LDH were observed in the FF group. The concentrations of FFA both in serum and myocardial tissue were markedly decreased in the FF group, while the expressions of PPARa, M-CPT-I and MCAD mRNA were increased （vs Iso, P〈0.01）. Conclusions The utilization of FFA was reduced in isoproterenol induced acute myocardial damage. PPARa activation by its activator fenofibrate may play a key role in energy metabolism in acute myocardial damage induced by isoproter
