CAJ | 학술논문

目的：从离子通道水平，观察雌激素（17α-ethynylestradiol and 17β-estradiol）对小鼠心室肌细胞ATP敏感性钾离子通道的影响。方法利用急性酶解法分离小鼠心室肌细胞，采用膜片钳制技术细胞膜内向外及细胞吸附记录模式。结果在钳制电压-60 mV细胞膜内向外记录模式下，向浴液中加入0.1μmol／L、1μmol／L及10μmol／L三种不同浓度雌激素，观察到两种雌激素（17α-ethynylestradiol、17β-estradiol）均对KATP通道有抑制作用，而且呈浓度依赖性，其半数有效浓度分别为0.3μmol／L 及0.1 nmol／L。在钳制电压-60mV细胞吸附记录模式下，向浴液中加入pinacidil或2，4-dinitrophenol （ DNP）活化KATP通道后，观察3 min，通道活性未见明显影响。在钳制电压-60mV细胞膜内向外记录模式下，向浴液中加入phorbol 12，13-dibutyrate（PDBu）0.001 nmol与处理后，观察到雌激素（10-8、10-3和1μmol／L）对于KATP离子通道活性抑制作用减弱。结论雌激素可通过影响心肌细胞KATP通道活性防止心律失常的产生，从而发挥心肌保护作用。
목적：종리자통도수평，관찰자격소（17α-ethynylestradiol and 17β-estradiol）대소서심실기세포ATP민감성갑리자통도적영향。방법이용급성매해법분리소서심실기세포，채용막편겸제기술세포막내향외급세포흡부기록모식。결과재겸제전압-60 mV세포막내향외기록모식하，향욕액중가입0.1μmol／L、1μmol／L급10μmol／L삼충불동농도자격소，관찰도량충자격소（17α-ethynylestradiol、17β-estradiol）균대KATP통도유억제작용，이차정농도의뢰성，기반수유효농도분별위0.3μmol／L 급0.1 nmol／L。재겸제전압-60mV세포흡부기록모식하，향욕액중가입pinacidil혹2，4-dinitrophenol （ DNP）활화KATP통도후，관찰3 min，통도활성미견명현영향。재겸제전압-60mV세포막내향외기록모식하，향욕액중가입phorbol 12，13-dibutyrate（PDBu）0.001 nmol여처리후，관찰도자격소（10-8、10-3화1μmol／L）대우KATP리자통도활성억제작용감약。결론자격소가통과영향심기세포KATP통도활성방지심률실상적산생，종이발휘심기보호작용。
Objective To study the effects of estrogens ( 17α-ethynylestradiol and 17β-estradiol ) on the ATP-sensitive potassium channel ( KATP ) activities in the enzymatically ( collagenase and protease ) isolated ICR mouse ventricular cardiomyocytes using inside-out and cell-attached patch clamp techniques .Methods In the inside-out patch configurations, the two estrogens reduced the K ATP channel activities in a dose-dependent manner at -60 mV holding potential ( HP) .Results The half-maximal inhibitory concentration ( IC50 ) of the 17α-esthynylestradiol and the 17β-estradiol were 0.3μmol/L and 0.1 nmol/L, respectively.However, these agents had no effects on the pinacidil-and DNP-induced KATP channel activities in the cell-attached patch configuration.However, the inhibitory effect of KATP channel activities by the 17-estrogens or the anti-estrogens in the excised inside-out patch configuration were abolished by 1 pmol/L PDBu.Conclusions The results of this study demonstrate that some estrogens decrease the K ATP channel activity acting on the inside of the isolated cardiomyocytes , and play a protective role to cardiomyocytes .