Objective：To focus on the asthmatic pathogenesis and clinical manifestations related to epithelial sodium channel （ENaC）/chlorine ion channel.Data Sources：The data analyzed in this review were the English articles...Objective：To focus on the asthmatic pathogenesis and clinical manifestations related to epithelial sodium channel （ENaC）/chlorine ion channel.Data Sources：The data analyzed in this review were the English articles from 1980 to 2015 from journal databases,primarily PubMed and Google Scholar.The terms used in the literature search were：（1） ENaCs;cystic fibrosis （CF） transmembrane conductance regulator （CFTR）;asthma/asthmatic,（2） ENaC/sodium salt;CF;asthma/asthmatic,（3） CFTR/chlorine ion channels;asthma/asthmatic,（4） ENaC/sodium channel/scnn1a/scnn1b/scnn1g/scnn1d/amiloride-sensitive/amiloride-inhibtable sodium channels/sodium salt;asthma/asthmatic,lung/pulmonary/respiratory/tracheal/alveolar,and （5） CFTR;CF;asthma/asthmatic （ti）.Study Selection：These studies included randomized controlled trials or studies covering asthma pathogenesis and clinical manifestations related to ENaC/chlorine ion channels within the last 25 years （from 1990 to 2015）.The data involving chronic obstructive pulmonary disease and CF obtained from individual studies were also reviewed by the authors.Results：Airway surface liquid dehydration can cause airway inflammation and obstruction.ENaC and CFTR are closely related to the airway mucociliary clearance.Ion transporters may play a critical role in pathogenesis of asthmatic exacerbations.Conclusions：Ion channels have been the center of many studies aiming to understand asthmatic pathophysiological mechanisms or to identify therapeutic targets for better control of the disease.展开更多
目的布比卡因是长效酰胺类局麻药,本研究旨在观察布比卡因对人肺上皮细胞短路电流的影响,并探讨可能的机制。方法应用尤斯灌流室装置测定H441单层细胞的短路电流。由总电流减去阿米洛利抑制后的电流算得阿米洛利敏感性电流,以用药前H44...目的布比卡因是长效酰胺类局麻药,本研究旨在观察布比卡因对人肺上皮细胞短路电流的影响,并探讨可能的机制。方法应用尤斯灌流室装置测定H441单层细胞的短路电流。由总电流减去阿米洛利抑制后的电流算得阿米洛利敏感性电流,以用药前H441单层细胞的阿米洛利敏感性电流初始值为100%对照。用100μmol·L^(-1)布比卡因处理H441细胞,在0、15、30、60 min 4个时间点提取蛋白用于Western blot,研究布比卡因对ERK1/2蛋白磷酸化的影响。结果布比卡因能够剂量依赖性抑制H441单层细胞的短路电流,此电流可被阿米洛利抑制;Western blot结果显示,布比卡因能够促进ERK1/2蛋白磷酸化。结论布比卡因通过抑制人肺上皮细胞阿米洛利敏感性电流而降低肺泡上皮离子转运,其机制可能与其促进ERK1/2蛋白磷酸化有关。临床上对伴有肺部疾患的病人应用布比卡因时应考虑其可能对肺泡上皮液体清除的影响。展开更多
目的探讨精氨酸抗利尿激素(AVP)对急性肺损伤肺水肿液清除作用。方法 48只健康成年的雄性SD大鼠随机分为对照组、模型组(ALI组)、AVP组,观察各组肺组织病理形态学、肺水含量、肺泡上皮通透性及肺泡液体清除率(AFC)变化,测定肺泡上皮钠通...目的探讨精氨酸抗利尿激素(AVP)对急性肺损伤肺水肿液清除作用。方法 48只健康成年的雄性SD大鼠随机分为对照组、模型组(ALI组)、AVP组,观察各组肺组织病理形态学、肺水含量、肺泡上皮通透性及肺泡液体清除率(AFC)变化,测定肺泡上皮钠通道(ENa C)和钠/钾ATP酶(Na+,K+-ATPase)表达情况。结果经AVP治疗后,模型组肺泡上皮通透性(0.27±0.15 vs0.59±0.19)及肺水含量(5.01±1.59 vs 8.67±1.79)减轻,AFC增加(23.56±4.51 vs 8.28±3.57),α-ENa C(1.296±0.322 vs 0.349±0.141)和α1-Na+,K+-ATPase表达增加(1.421±0.389 vs 0.338±0.186),均有显著差异(P<0.05)。结论 AVP能促进AFC,其作用途径可能是上调α-ENa C和α1-Na+,K+-ATPase通道蛋白实现的。展开更多
基金grants from American Heart Association grant （No. 20130034） and National Natural Science Foundation of China （No. 21307158）.
文摘Objective：To focus on the asthmatic pathogenesis and clinical manifestations related to epithelial sodium channel （ENaC）/chlorine ion channel.Data Sources：The data analyzed in this review were the English articles from 1980 to 2015 from journal databases,primarily PubMed and Google Scholar.The terms used in the literature search were：（1） ENaCs;cystic fibrosis （CF） transmembrane conductance regulator （CFTR）;asthma/asthmatic,（2） ENaC/sodium salt;CF;asthma/asthmatic,（3） CFTR/chlorine ion channels;asthma/asthmatic,（4） ENaC/sodium channel/scnn1a/scnn1b/scnn1g/scnn1d/amiloride-sensitive/amiloride-inhibtable sodium channels/sodium salt;asthma/asthmatic,lung/pulmonary/respiratory/tracheal/alveolar,and （5） CFTR;CF;asthma/asthmatic （ti）.Study Selection：These studies included randomized controlled trials or studies covering asthma pathogenesis and clinical manifestations related to ENaC/chlorine ion channels within the last 25 years （from 1990 to 2015）.The data involving chronic obstructive pulmonary disease and CF obtained from individual studies were also reviewed by the authors.Results：Airway surface liquid dehydration can cause airway inflammation and obstruction.ENaC and CFTR are closely related to the airway mucociliary clearance.Ion transporters may play a critical role in pathogenesis of asthmatic exacerbations.Conclusions：Ion channels have been the center of many studies aiming to understand asthmatic pathophysiological mechanisms or to identify therapeutic targets for better control of the disease.
文摘目的布比卡因是长效酰胺类局麻药,本研究旨在观察布比卡因对人肺上皮细胞短路电流的影响,并探讨可能的机制。方法应用尤斯灌流室装置测定H441单层细胞的短路电流。由总电流减去阿米洛利抑制后的电流算得阿米洛利敏感性电流,以用药前H441单层细胞的阿米洛利敏感性电流初始值为100%对照。用100μmol·L^(-1)布比卡因处理H441细胞,在0、15、30、60 min 4个时间点提取蛋白用于Western blot,研究布比卡因对ERK1/2蛋白磷酸化的影响。结果布比卡因能够剂量依赖性抑制H441单层细胞的短路电流,此电流可被阿米洛利抑制;Western blot结果显示,布比卡因能够促进ERK1/2蛋白磷酸化。结论布比卡因通过抑制人肺上皮细胞阿米洛利敏感性电流而降低肺泡上皮离子转运,其机制可能与其促进ERK1/2蛋白磷酸化有关。临床上对伴有肺部疾患的病人应用布比卡因时应考虑其可能对肺泡上皮液体清除的影响。
文摘目的探讨精氨酸抗利尿激素(AVP)对急性肺损伤肺水肿液清除作用。方法 48只健康成年的雄性SD大鼠随机分为对照组、模型组(ALI组)、AVP组,观察各组肺组织病理形态学、肺水含量、肺泡上皮通透性及肺泡液体清除率(AFC)变化,测定肺泡上皮钠通道(ENa C)和钠/钾ATP酶(Na+,K+-ATPase)表达情况。结果经AVP治疗后,模型组肺泡上皮通透性(0.27±0.15 vs0.59±0.19)及肺水含量(5.01±1.59 vs 8.67±1.79)减轻,AFC增加(23.56±4.51 vs 8.28±3.57),α-ENa C(1.296±0.322 vs 0.349±0.141)和α1-Na+,K+-ATPase表达增加(1.421±0.389 vs 0.338±0.186),均有显著差异(P<0.05)。结论 AVP能促进AFC,其作用途径可能是上调α-ENa C和α1-Na+,K+-ATPase通道蛋白实现的。
