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作 者:葛敏[1] 单锋[1,2] 唐碧[3] 侯秀杰[4]
机构地区:[1]蚌埠医学院药学系,安徽蚌埠233030 [2]合肥市第四人民医院药剂科,安徽合肥230022 [3]蚌埠医学院第一附属医院心血管科,安徽蚌埠233004 [4]阜阳市第一人民医院心血管科,安徽阜阳236000
出 处:《中国应用生理学杂志》2016年第2期128-131,136,共5页Chinese Journal of Applied Physiology
基 金:国家自然科学基金资助项目(81170046);教育部留学回国人员科研启动基金(第46批);安徽省自然科学基金资助项目(10040606Q44)
摘 要:目的:探讨二十二碳六烯酸(DHA)对大鼠心房颤动(AF)模型心房肌生理特性的影响及相关机制研究。方法:80只乙酰胆碱-氯化钙混合液敏感的SD大鼠分为对照组(CTL组)、DHA处理组(DHA组)、房颤组(AF组)和房颤+DHA处理组(DHA+AF组),观察房颤持续时间;采用全细胞膜片钳技术记录大鼠心房肌细胞动作电位时程(APD)和双孔钾通道TASK-1电流,Western blot测定大鼠心房组织TASK-1蛋白表达。结果:大鼠尾静脉注射乙酰胆碱-氯化钙混合液后,房颤持续时间随实验天数增加而逐渐延长,DHA干预缩短房颤持续时间。与CTL组相比,AF组大鼠心房肌细胞复极50%时的动作电位时程(APD50)和复极90%时的动作电位时程(APD90)明显缩短,心房肌细胞TASK-1电流密度升高,蛋白表达升高(P<0.05)。与AF组相比,DHA+AF组大鼠心房肌细胞APD50和APD90明显延长,TASK-1电流密度和蛋白表达降低(P<0.05)。结论:DHA具有延长房颤大鼠心房肌细胞APD的作用,可能与其下调心房肌TASK-1蛋白的表达从而降低心房肌细胞TASK-1电流密度有关。Objective: To investigate the effect of docosahexaenoic acid (DHA) on atrial physiological parameter and its related mechanisms in atrial fibrillation rats. Methods: Eighty Sprague-Dawley (SD) rats which were sensitive to acetylcholine-calcium chloride mixture were randomly divided into four groups: control (CTL), control treated with DHA (DHA), atrial fibrillation (AF) and atrial fibrillation treated with DHA (DHA + AF). The duration of atrial fibrillation was measured. The atrial myocyte action potential duration (APD) and TWIK-related acid-sensitive K+ channels-1 (TASK-1) currents were recorded by whole-cell patch-clamp technique. The expression of TASK-1 at protein level in atrial tissue was detected by Western blot method. Results: Atrial fibrillation of the rats was induced by acetylcholine-calcium chloride mixture, and the duration time of atrial fibrillation was increased with the drug-induced time prolonged. Compared with control group, the time of atrial myocyte action potential duration at 50% repolarization (APD50) and at 90% repolarization (APD90) were significantly shorten in AF group, TASK- 1 current density and TASK- 1 protein expression were increased ( P 〈 0.05). Compared with AF group, the duration of atrial fibrillation was decreased, the time of atrial myocyte APD50 and APD90 were prolonged, TASK- 1 current density and protein expression were significantly reduced in DHA + AF group ( P 〈 0.05). Conclusion: DHA can prolong the atrial myocyte APD in atrial fibrillation rats, which may be related to down-regulation of TASK-1 protein expression and decreasing TASK-1 current density in atrial tissue.
关 键 词:心房颤动 二十二碳六烯酸 心房电重构 TASK-1 大鼠
分 类 号:R541.75[医药卫生—心血管疾病]
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