Tu T Y, Amiel C, Tran Ba Huy P, Herman P
Laboratoire d'Otologie Expérimentale, Faculté Lariboisière-St-Louis, Paris, France.
Acta Otolaryngol. 1995 Mar;115(2):291-5. doi: 10.3109/00016489509139312.
Primary cultures of middle ear (ME) epithelial cells from gerbils were used to investigate the effect on ion transport of reactive oxygen species (ROS), which are major inflammatory mediators. Short-circuit current measurements revealed an unexpected result: low concentrations of ROS induced an increase in transepithelial sodium transport. This stimulation was mediated by the endogenous synthesis of prostaglandin E2, which in turn increased the intracellular adenosine 3',5'-cyclic monophosphate (cAMP) content. This effect was blunted by indomethacin. By stimulating sodium and fluid transport, ROS may reduce the depth of the periciliary fluid layer, and may thus be involved in the impairment of mucociliary clearance which initiates chronic otitis media.
用沙土鼠中耳（ME）上皮细胞的原代培养物来研究活性氧（ROS）对离子转运的影响，活性氧是主要的炎症介质。短路电流测量揭示了一个意外的结果：低浓度的活性氧会导致跨上皮钠转运增加。这种刺激是由前列腺素E2的内源性合成介导的，而前列腺素E2又会增加细胞内3',5'-环磷酸腺苷（cAMP）的含量。吲哚美辛可减弱这种作用。通过刺激钠和液体转运，活性氧可能会减少纤毛周围液层的深度，因此可能参与引发慢性中耳炎的黏液纤毛清除功能障碍。
