【摘要】 目的探讨巴豆醛对小鼠气管上皮及原代培养单层气管上皮细胞短路电流的影响及其与PKG2之间的关系,明确巴豆醛在呼吸系统液体转运中可能的作用机制。方法应用尤斯灌流装置记录小鼠气管上皮及原代培养单层气管上皮细胞短路电流,采用Elisa实验明确巴豆醛对ENa C活性的影响。结果巴豆醛能够抑制小鼠气管上皮和原代培养的单层气管上皮细胞的阿米洛利敏感性短路电流,而此阿米洛利敏感性肺液清除主要是由ENa C介导的液体转运。Elisa实验进一步明确了巴豆醛通过抑制PKG2而参与ENa C活性的调控作用。结论巴豆醛可能通过抑制呼吸系统ENa C的功能,阻碍Na+的重吸收,通过抑制PKG2而参与ENa C活性的调控作用,进而诱导产生肺水肿或急性呼吸窘迫综合征。更多还原

【Abstract】 Objective To investigate the effect of crotonaldehyde on short circuit currents in tracheal epithelium and primary cultured tracheal epithelial monolayer of mice and its relationship with PKG2,and to clarify the possible mechanism of the action of crotonaldehyde on respiratory fluid transport. Methods Application of Ussing chamber for recording mouse tracheal epithelial and primary cultured tracheal epithelial cell monolayer short-circuit current,using Elisa experiment for measuring ENa C activity by crotonaldehyde.Results The amiloride sensitive short-circuit currents of mouse trachea and primary cultured monolayer epithelial cells can be inhibited by crotonaldehyde,which is mainly mediated by ENa C. Elisa experiments further confirmed that PKG2 was involved in the regulation of ENa C activity by crotonaldehyde. Conclusion Crotonaldehyde may inhibit the reabsorption of Na+by inhibiting the function of respiratory system ENa C through PKG2 regulation,and then induce pulmonary edema or acute respiratory distress syndrome.更多还原