Herman P, Tan C T, van den Abbeele T, Escoubet B, Friedlander G, Huy P T
Laboratoire d'Otologie Expérimentale, Faculté Lariboisiere, St. Louis, Université Paris VII, France.
Am J Physiol. 1997 Jan;272(1 Pt 1):C184-90. doi: 10.1152/ajpcell.1997.272.1.C184.
The effect of glucocorticosteroids on ion transport was investigated on a middle ear cell line with the short-circuit current (Isc) technique. Dexamethasone (DXM) produced a dose- and time-dependent increase in Isc. Concentration of half-maximal stimulation was 2.68 x 10(-8) M. This effect was blunted by the glucocorticoid antagonist RU-38486 and was related to Na+ transport, as evidenced by the inhibition induced by 1) apical addition of the Na+ channel inhibitor benzamil (10(-6) M) or 2) substitution of Na+ with N-methylglucamine in the incubation medium. The increase in Na+ transport resulted from a primary modulation of apical Na+ entry, since 1) the Na(+)-K(+)-ATPase activity of cellular homogenates was not modified by corticosteroids and 2) the DXM-induced increase in the ouabain-sensitive uptake of 86Rb was blunted by benzamil. Ribonuclease protection assay revealed 1) a constitutive expression of the mRNA encoding the alpha-subunit of the epithelial Na+ channel and 2) that DXM increased the expression of this transcript. This increase was dose dependent and paralleled changes in transepithelial Na+ transport. This study suggests that a component of the beneficial effect of steroid therapy for the treatment of otitis media might be related to increased fluid clearance.
采用短路电流（Isc）技术，在一种中耳细胞系上研究了糖皮质激素对离子转运的影响。地塞米松（DXM）使Isc呈剂量和时间依赖性增加。半数最大刺激浓度为2.68×10⁻⁸ M。糖皮质激素拮抗剂RU - 38486减弱了这种作用，且该作用与Na⁺转运有关，这一点可通过以下现象得以证明：1）在顶端加入Na⁺通道抑制剂苄amil（10⁻⁶ M）或2）在孵育培养基中用N - 甲基葡糖胺替代Na⁺所诱导的抑制作用。Na⁺转运的增加源于顶端Na⁺内流的原发性调节，因为1）细胞匀浆的Na⁺ - K⁺ - ATP酶活性未被皮质类固醇改变，且2）苄amil减弱了DXM诱导的哇巴因敏感的⁸⁶Rb摄取增加。核糖核酸酶保护试验显示：1）编码上皮Na⁺通道α亚基的mRNA的组成性表达，以及2）DXM增加了该转录本的表达。这种增加呈剂量依赖性，且与跨上皮Na⁺转运的变化平行。本研究提示，类固醇疗法治疗中耳炎的有益作用的一个组成部分可能与液体清除增加有关。
