中文摘要：

目的：探讨心肌SarcKATP通道h6．2在运动预适应心肌保护效应中的变化以及与PKC的关系。方法：SD大鼠分对照组（C组）、力竭运动组（EE组）、运动预适应组（EP纽）、运动预适应＋力竭运动组（EP＋EE组）、PKC阻断剂＋运动预适应组（CHE＋EP）和PKC阻断剂十运动预适应＋力竭运动组（CHE＋EP＋EE组）。一次大强度间歇跑台运动建立运动预适应模型，力竭跑台运动致大鼠心肌损伤。用原位杂交和实时荧光定量PCR法检测kr6．2mRNA变化，用免疫荧光和免疫印迹法检测kir6．2蛋白变化。结果：与C组比，EE组和EP组kir6．2mRNA无明显变化，而EE组kir6．2蛋白明显升高，EP组kir6．2蛋白明显下降。与EE组比，EP＋EE组kir6．2mRNA无明显变化，1（ir6．2蛋白明显下降。与EP组比，CHE＋EP组kir6．2mRNA明显降低，kir6．2蛋白明显升高。与EP＋EE组比，CHE＋EP＋EE组kr6．2mRNA和kir6．2蛋白无明显变化。结论：在EP诱导的保护效应中，心肌SarCKATI，通道kir6．2mRNA水平未发生明显变化，而kir6．2蛋白水平明显降低，提示，心肌SarCKATP通道通过kir6．2蛋白水平的降低介导EP诱导的心肌保护效应。PKC对心肌SarcKare通道的表达具有调控作用。

英文摘要：

Objective= To study the changes of the Pore-Forming Subunit kir6. 2 of myocardial sarcolernmal ATP-sensitive potassium （SarCKATe） channels in myocardial protection of exercise preconditioning （EP） and the relations with protein kianse C （PKC）. Methods： SD rats were divided into control group （ C）, EE group, EP group, EP ＋ EE group, CHE ＋ EP group and CHE＋EP＋ EE group. By using once heavy intensity interval treadmill running, this paper es- tablishes EP model, and exhaustive exercise on treadmill to induce rats myocardial injury. In-si- tu hybridization and real-time fluorescence quantitative PCR methods were used to detect chan- ges of kir6. 2 rnRNA. Immunofluorescence and westten blotting methods were used to detect changes of kir6. 2 protein. Results： Compared with group C, there is no significant change of kir6.2 MRNA in group EE and EP, while kir6. 2 protein significantly increased in group EE and significantly decreased in group EP. Compared with group EE, no significant changes of kit6.2 mRNA in group EP ＋ EE, kit6. 2 protein in group EPq-EE significantly decreased. Compared with group EP, kir6. 2 mRNA significantly decreased in group CHE＋EP, kir6. 2 protein significantly increased in group CHE＋EP. Compared with group EP＋ EE, there is no significant changes of kir6. 2 mRNA and kir6. 2 protein in group CHE＋EP＋EE. Conclu- sion：In myocardial protection induced by EP, kir6. 2 mRNA did not changed significantly, while kit6.2 protein decreased significantly, which demonstrated myocardial SarCKATP channels mediated myocardial protection induced by EP through kir6.2 protein decreased. PKC can reg- ulate expression of myocardial SarcKATP channels.