Regulation of IGF System in Rats after Experimental Myocardial Infarction / 체질인류학회지

Insulin-like growth factor system (IGF system) has been reported to be associated with the variety of disorders of myocardial function. However, the effect of myocardial infarction (MI) on the IGF system has not been fully described. Thus, the present study was to investigate in more detail the changes of IGF system in the male rat following myocardial infarction (MI). Ligation of the left coronary artery was performed in male Sprague-Dawley male rats at 60 days of age. Control rats were obtained sham-operated animals. MI rats were sacrificed at 1, 3, 7, 14, and 30 day after ligation of left anterior descending coronary artery. Control rats were sacrificed on 30 day after thoracotomy. Myocardial infarct size was assessed by planimetry and perimetry. Serum and heart concentrations of IGF-I and -II were determined by radioimmunoassay. Serum levels of IGF-binding protein (IGFBP)-1 and IGFBP-3 were analyzed with a two-site immunoradiometric assay. Mean infarct size was 35.2~42.3% of the left ventricle after coronary occlusion in experimental groups. Serum levels of IGF-I were markedly reduced, but the levels of IGF-II were not altered in MI rats compared with shamligated controls. Serum IGFBP-I levels in MI rats were significantly increased at 1 and 3 day compared with sham rats. The levels of serum IGFBP-3 were significantly higher in the ligated rats. IGF-I levels of the infarct/periinfarct area of the left ventricle were significantly decreased in rats with myocardial infarction, whereas the levels of IGF-II remained unchanged. These results demonstrate that the IGF system is altered in the myocardial infarction and suggest that the IGF system plays an important role in the response of the heart to myocardial infarction.

The Effects of Ischemic Preconditioning and K(ATP) channel Activation on the Expression of the PKC-epsilon, NF-kappaB and AP-1 in Ischemia-reperfused Rat Heart / 체질인류학회지

This study was aimed to elucidate the effects of K(ATP) activation during IPC on the PKC-epsilon, NF-kappaB and AP-1 in ischemia-reperfused rat hearts. SD male rats weighting from 300 to 350 g were split into 9 groups, such as sham control (S), IPC, 3 cycles of 5 min ischemia and 5 min reperfusion, continuous preconditioning (CP), 8 cycles of 5 min ischemia and 5 min reperfusion, K(ATP) opening (KO) with pinacidil (1.0 mg/kg), K(ATP) blocking with glibenclamide (1.0 mg/kg) injection, ischemia (IS), 30 min ischemia, IPC followed by IS, 8) K(ATP) blocking and IPC followed by IS (KB+IPC+IS), IS and K(ATP) opening (KO+IS). Heart were subjected to ligation of left descending coronary artery and reperfusion in groups of IPC, CP, IS with or without IPC. Immunohistochemistry and Western blotting for PKC-epsilon, NF-kappaB and AP-1 were performed at 3, 6, 24 hours after reperfusion or treatment. Immunoreactivities against PKC-epsilon antibody were observed stronger in the groups of IPC, KO, IPC+IS and KO+IS than groups of KB, IS and KB+IPC+IS. NF-kappaB activation and translocation were only observed in the groups of including 30 min ischemia and reperfusion. AP-1 activation and translocation were opposite to the results of PKC-epsilon activation. In the group of CP, KB, IS and KB+IPC+IS, reactivities of AP-1 antibody were stronger than IPC+IS, KO+IS, and weaker in the groups of S, IPC and KO. These results suggest that K(ATP) opening with IPC or pharmacological methods may direct effect on the PKC-epsilon activation and that K(ATP) blocking has effect on the AP-1 activation and translocation in the heart of ischemiareperfused of rats.