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Effects of Ischemic Preconditioning and K ATP Channel on the PKC ε Activation in Rat Heart
Author(s) -
Paik Doojin,
Jeon Sukyoung,
Ha Jaehyun,
Ahn Dongchoon
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a26-d
Subject(s) - glibenclamide , protein kinase c , ischemic preconditioning , pinacidil , blot , ischemia , medicine , chemistry , immunohistochemistry , endocrinology , pharmacology , anesthesia , kinase , biochemistry , gene , diabetes mellitus
The K ATP channel opening and the PKC activation are the major triggers in protective effects of ischemic preconditioning. This study is aimed to clarify the relationship between K ATP channel and the PKC activation in ischemic preconditioning in the rat heart. The possible effect of K ATP channel opening on PKC ε activation in the rat heart was examined by immunohistochemistry and western blotting at 3, 6, 24 hours after reperfusion or treatment. Pinacidil (1mg/kg)(KO) and glibenclamide (0.5mg/kg)(KB) were used for K ATP channel opening or blocking. The hearts were subject to sham operation(S), ischemic preconditioning (3 cycles of 5 minutes ischemia followed by 5 minute reperfusion: IPC). On immunohistochemistry at 3 hours, strong reaction(+++) of PKC ε was observed in the IPC group, weak reaction (+) in KO alone groups, but no reaction in S, KB+IPC and KB groups except 24 hours in KB+IPC. On Western blotting, PKC ε was decreased significantly in the KB+IPC, KB alone groups except at 24 hours in KB+IPC which insignificant reduction. But, no reduction in IPC and KO groups. These results suggest the K ATP channel opening and blocking in ischemic preconditioning might effect on PKC ε activation.