허혈양상화와 KATP 이온통로 활성이 허혈-재관류된 흰쥐 심장에서 PKC-ε, NF-κB와 AP-1발현에 미치는 영향

초록

This study was aimed to elucidate the effects of KATP activation during IPC on the PKC-ε, NF-κB 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, KATP opening (KO) with pinacidil (1.0 mg/kg), KATP blocking with glibenclamide (1.0 mg/kg) injection, ischemia (IS), 30 min ischemia, IPC followed by IS, 8) KATP blocking and IPC followed by IS (KB+IPC+IS), IS and KATP 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-ε, NF-κB and AP-1 were performed at 3, 6, 24 hours after reperfusion or treatment. Immunoreactivities against PKC-ε 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-κB 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-ε 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 KATP opening with IPC or pharmacological methods may direct effect on the PKC-ε activation and that KATP blocking has effect on the AP-1 activation and translocation in the heart of ischemiareperfused of rats.

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