中文摘要：

目的：观察Syn-1A在抑制弱酸性pH诱导的KATP通道活化过程中的作用及机制。方法：用稳定表达Kir6.2/SUR2A KATP通道的HEK-293细胞构建细胞膜内面向外的记录方式,并给细胞膜片连续灌流含或不含Syn-1A的pH7.4,7.0,6.8,6.5和6.0的溶液,观察弱酸性pH对通道的活化作用及Syn-1A对上述作用的抑制,并采用体外结合实验分析不同pH对Syn-1A与SUR2A亚单位结合的影响。结果：Syn-1A可抑制pH 6.5,6.8和7.0时诱发的通道活化作用,Syn-1A与SUR2A的结合在pH7.4至6.0范围内,随pH下降逐渐增加。结论：Syn-1A对KATP通道的抑制作用可缓冲pH波动引起的KATP通道开放,从而抑制折返性心律失常的发生。

英文摘要：

Aim： To investigate the action and mechanism of Syn-lA in reversing the activation of KATP channel induced by weak acidic pH. Methods： The patches excised from Kir6.2/SUR2A expressing HEK-293 cells were used to establish inside-out configuration. To exa mine the actions of weak acidic pH in activation of the channel and the reverse action of Syn-lA on it, the inside-out pacthes were continuously perfused with the solution of pH from 7.4, 7.0, 6.8, 6.5 to 6.0 with or without Syn-lA. In vitro binding was employed to study the influence of different pH to the binding of Syn-1A to SUR2A subunit. Results： Syn-lA blocked pH6.5, 6.8 and 7.0 induced activation of the channel, and Syn-lA binding to SUR2A were increased by reducing pH from 7.4 to 6.0. Conclusion： Syn-lA would assert some inibition of the KATP channels, which might temper the fluctuation of acidic pH-induced KA-rP channel opening that could induce fatal re-entrant arrhythmias.