Research On Changes Of Myocardial ATP-sensitive Potassium Channels In Cardioprotection Induced By Exercise Preconditioning Of Relieving Athletic Myocardial Injury

Objective: Sports medicine pays closely attention to powerfulcardioprotection induced by exercise preconditioning （EP） increasingly. Themechanism of EP cardiopretection possiblely comes down to triggermaterial, intermidiay material and effect material cell signal transductionpathways. On the basis of EP cardioprotection of relieving athleticmyocardial injury caused by exhaustive exercise, this study has probed intothe changes of myocardial K_ATPchannels subnit kir6.2and SUR2A incardioprotection induced by EP. Meanwhile, it probed into the effect ofPKC on myocardial K_ATPchannel expressional regulation by using PKCinhibitor chelerythrine chloride （CHE）, in order to provide newer guide andthought for the study of the mechanism of EP.Methods: SD mice were divided into10groups randomly: C group, EEgroup, EEP group, CHE+EEP group, EEP+EE group, CHE+EEP+EE group,LEP group, CHE+LEP group, LEP+EE group, CHE+LEP+EE group. Usehigh intensity treadmill running to esteblish EP mode, and athleticmyocardial injury caused by exhaustive treadmill running. The changes ofmyocardial structure of the mice were observed by hematoxylin erosin（HE）coloration, and the changes of myocardial lacking of blood and oxygen byhaematoxylin basie fuchsin picric acid（HBFP）coloration.The content ofcTnI is tested by immunochemistic shining method and content of theN-terminalpro-brain natriuretic peptide （NT-proBNP） by enzyme linkedimmunnosorbent assay. In order to evaluate the changes of myocardialstructure form and function after athletic myocardial injury, and observe theeffect of cardioprotection induced by EP. The distribution of myocardialkir6.2mRNA and SUR2A mRNA of the mice were observerd by means ofin-situ hybridization and the changes of it were tested by means of realtimefluorescence quantitative PCR. The protein distribution of kir6.2andSUR2A were observed by means of Immunofluorescence and the changes ofthe protein of kir6.2and SUR2A were tested by the means of westernblotting. Meanwhile, use PKC inhibitor CHE to disclose the influence ofPKC on the expressional regulation of kir6.2and SUR2A in cardioprotection induced by EP.Results:（1）Compared with group C, the content of cTnI and NT-proBNPof the mice in group EE increased significantly, and myocardial fiberbending deformation, meanwhile with myocardial ischemic-anoxia seriously.Compared with group EE, the content of cTnI and NT-proBNP decreasedsignifisantly in group EEP+EE, and with myocardial ischemic-anoxialightened. The content of NT-proBNP has little changed in group LEP+EE,and the content of cTnI decreased signifisantly in group LEP+EE,meanwhile with myocardial ischemic-anoxia seriously.（2）Compared withgroup C, the expression of kir6.2mRNA did not changed significantly ingroup EEP and LEP. The expression of kir6.2protein did not changedsignificantly in group LEP, but decreased significantly in group EEP; Theexpression of SUR2A mRNA has an uptrend in group EEP and LEP. Theexpression of SUR2A protein did not changed significantly in group EEP,but decreased significantly in group LEP; The expression of kir6.2mRNAtends to decline in group EE. The expression of kir6.2protein increasedsignificantly in group EE. SUR2A mRNA and SUR2A protein increasedobviously in group EE. Compared with group EE, the expression of kir6.2mRNA tends to decline and the expression of kir6.2protein declinedobviously in group EEP+EE and LEP+EE. The expression of SUR2A mRNAdeclined obviously in group EEP+EE and tends to decline in group LEP+EE.The expression of SUR2A protein declined obviously in group EEP+EE andLEP+EE（.3）Compared with group EEP, in group CHE+EEP, the expressionof kir6.2mRNA declined obviously, The expression of kir6.2proteinincreased obviously, The expression of SUR2A mRNA tends to decline andthe expression of SUR2A protein declined obviously. Compared with groupEEP+EE, in group CHE+EEP+EE, the expression of kir6.2mRNA tends todecline, as well as the expression of the of kir6.2protein, The expression ofSUR2A mRNA and the expression of SUR2A protein both increasedobviously. Compared with group LEP, in group CHE+LEP, the expression ofkir6.2mRNA and the expression of kir6.2protein tend to decline, while theexpression of SUR2A mRNA tends to increase and the expression of SUR2Aprotein increased obviously. Compared with group LEP+EE, in groupCHE+LEP+EE, the expression of kir6.2mRNA and SUR2A proteinincreased obviously, while the expression of the protein of kir6.2proteinand SUR2A mRNA tends to decline.Conclusion:（1）Exhaustive exercise causes athletic myocardial injury tothe mice, and exercise preconditioning （EP） induced cardioprotection of relieving the athletic myocardial injury.（2）kir6.2mRNA did not changedobviously in cardioprotection induced by EP, while SUR2A mRNA changedsignificantly. At the same time, kir6.2and SUR2A protein decreasedobviously in EP cardioprotection. Pointed out that myocardial K_ATPchannels participate in the cardioprotection of relieving athletic myocardialinjury through the changes of kir6.2and SUR2A.（3）In cardioprotection ofrelieving athletic myocardial injury induced by EP, PKC regulated theexpression of K_ATPchannel subnit kir6.2and SUR2A, indicated that PKC isupper intermidary material of K_ATPchannel in the signal transferringapproach of cardioprotection induced by EP. PKC inhibitor CHE causes thediffirent changes of the expression of the K_ATPchannels subnit kir6.2andSUR2A, indicating that the regulating mechanism that PKC does to kir6.2and SUR2A may be diffirent. However, the specific mechanism needs toexplore more deeply.