Docosahexaenoic acid selectively augments muscarinic stimulation of epithelial Cl- secretion.
Docosahexaenoic acid selectively augments muscarinic stimulation of epithelial Cl- secretion.
复制标题
二十二碳六烯酸选择性地增强上皮Cl-分泌的毒蕈碱刺激。
DOI：
10.1016/s0022-4804(02)00092-6
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Matthews,JeffreyB
中科院分区：
文献类型：
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作者：
DelCastillo,IsabelCalvo;Alvarez,JuanG;Freedman,StevenD;Ollero,Mario;Claros,Leonardo;Song,JCecilia;Yoo,James;Matthews,JeffreyB
研究背景我们研究了各种脂肪酸对T84细胞（一种肠上皮细胞模型）的产电性氯分泌的影响。材料与方法采用常规电流-电压钳技术研究了生长在可渗透支持物上的T84细胞。从T84细胞中提取膜脂，甲基转移，并通过气相色谱法进行分析。通过amynopropil柱层析将脂质提取物分离成非极性、游离脂肪酸和磷脂。二十二碳六烯酸（DHA）而不是二十碳五烯酸或其他脂肪酸选择性地增强对毒蕈碱激动剂卡巴胆碱的分泌反应，但不增强对其他Ca 2+激动剂（组胺、毒胡萝卜素或离子霉素）的反应或对cAMP激动剂毛喉素的反应。DHA增加Cl−分泌的能力似乎与游离DHA水平的关系比与膜结合DHA的关系更密切。DHA对T84细胞的其他影响包括跨上皮阻力（屏障功能的测量）的减少，这些作用与Cl−分泌的影响无关。CONCLUSIONThe结果表明，DHA已被证明可以逆转实验性囊性纤维化中的器官病理学，可能选择性地影响激动剂调节的转运事件和上皮细胞的其他基本特性。
BACKGROUNDWe investigated the effect of various fatty acids on electrogenic chloride secretion in T84 cells, a model for intestinal epithelium.MATERIALS AND METHODST84 intestinal epithelial cells grown on permeable supports were studied by conventional current-voltage clamping. Membrane lipids from T84 cells were extracted, transmethylated, and analyzed by gas chromatography. Lipid extracts were fractionated into nonpolar, free fatty acids, and phospholipids by amynopropil column chromatography.RESULTSDocosahexaenoic acid (DHA) but not eicosapentanoic acid or other fatty acids selectively enhanced the secretory response to the muscarinic agonist carbachol but not the response to other Ca2+agonists (histamine, thapsigargin, or ionomycin) or the response to the cAMP agonist forskolin. The ability of DHA to augment Cl−secretion appeared to correlate closer with free DHA levels than with membrane-bound DHA. Other effects of DHA on T84 cells included a reduction in transepithelial resistance (a measure of barrier function), actions that were dissociated from the effect on Cl−secretion.CONCLUSIONThe results suggest that DHA, which has been shown to reverse organ pathology in experimental cystic fibrosis, may selectively affect agonist-regulated transport events and other fundamental properties of epithelial cells.