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首页> 外文期刊>Journal of Cellular Physiology >N-acetylcysteine inhibits Na(+) absorption across human nasal epithelial cells.
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N-acetylcysteine inhibits Na(+) absorption across human nasal epithelial cells.

机译：防治作用抑制Na(+)吸收人类鼻腔上皮细胞。

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摘要

N-acetylcysteine (NAC) is a widely used mucolytic drug in patients with a variety of respiratory disorders. The mechanism of action is based on rupture of the disulfide bridges of the high molecular glycoproteins present in the mucus, resulting in smaller subunits of the glycoproteins and reduced viscosity of the mucus. Because Na(+) absorption regulates airway surface liquid volume and thus the efficiency of mucociliary clearance, we asked whether NAC affects the bioelectric properties of human nasal epithelial cells. A 24-h basolateral treatment with 10 mM of NAC decreased the transepithelial potential difference and short-circuit current (I(SC)) by 40%, and reduced the amiloride-sensitive current by 50%, without affecting the transepithelial resistance. After permeabilization of the basolateral membranes of cells with amphotericin B in the presence of a mucosal-to-serosal Na(+) gradient (135:25 mM), NAC inhibited 45% of the amiloride-sensitive current. The Na(+)-K(+)-ATPase pump activity and the basolateral K(+) conductance were not affected by NAC treatment. NAC did not alter total cell mRNA and protein levels of alpha-epithelial Na(+) channel (EnaC) subunit, but reduced abundance of alpha-ENaC subunits in the apical cell membrane as quantified by biotinylation. This effect can be ascribed to the sulphydryl (SH) group of NAC, since N-acetylserine and S-carboxymethyl-l-cysteine were ineffective. Given the importance of epithelial Na(+) channels in controlling the thin layer of fluid that covers the surface of the airways, the increase in the fluidity of the airway mucus following NAC treatment in vivo might be in part related to downregulation of Na(+) absorption and consequently water transport. J. Cell. Physiol. 201: 106-116, 2004. Copyright 2004 Wiley-Liss, Inc.
机译：防治(NAC)是一种广泛使用的黏液溶解的药物患者的呼吸障碍。断裂二硫桥的高粘液糖蛋白分子存在,导致小的子单元糖蛋白和降低粘度的粘液。因为钠(+)吸收调节气道表面液体体积,因此效率黏膜纤毛的间隙,我们问南汽影响人类鼻腔的生物属性上皮细胞。10毫米的NAC transepithelial下降潜在的差异和短路电流(我(SC)) 40%,并减少了amiloride-sensitive当前的50%,影响transepithelial阻力。基底外侧膜的透化作用与两性霉素B细胞的存在mucosal-to-serosal Na(+)梯度(135:25毫米),南汽抑制amiloride-sensitive的45%电流。基底外侧K(+)电导受NAC治疗。总细胞信使rna和蛋白质的水平alpha-epithelial Na(+)通道亚基(钠),但减少大量的alpha-ENaC子单元量化的顶端细胞膜生物素酰化。巯基(SH)南汽集团N-acetylserine和S-carboxymethyl-l-cysteine是无效的。上皮钠(+)渠道控制薄层的液体覆盖的表面航空公司,增加的流动性NAC治疗体内后气道粘液可能的差别有关对这些基因的一部分Na(+)吸收,因此水交通工具。版权2004 Wiley-Liss公司。

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