山东医药
山東醫藥
산동의약
SHANDONG MEDICAL JOURNAL
2014年
14期
18-21
,共4页
李烁%钟国强%何艳%肖飞%蒋智渊%蒙滋滋
李爍%鐘國彊%何豔%肖飛%蔣智淵%矇滋滋
리삭%종국강%하염%초비%장지연%몽자자
心房颤动%M3受体%缝隙连接蛋白43
心房顫動%M3受體%縫隙連接蛋白43
심방전동%M3수체%봉극련접단백43
atrial fibrillation%M3 receptor%connexin 43
目的:探讨M3受体及Cx43在心房颤动发生与维持中的作用及二者之间的相互关系。方法收集94例风湿性心脏病瓣膜置换术患者右心房组织,按是否存在心房颤动分为心房颤动组( AF组,49例)和窦性心律组( SR组,45例),采用免疫荧光在激光共聚焦显微镜下观察M3受体和Cx43蛋白的表达及两者的结构共定位情况,采用Western blot方法检测两组M3受体和Cx43蛋白的蛋白表达量。结果与SR组相比,AF组心房组织M3受体及Cx43蛋白表达量下降(P<0.05),但M3受体与Cx43的结构共定位关系增强(P<0.05)。结论房颤患者右心房组织Cx43表达量下降,可能是房颤发生与维持机制之一,M3受体的表达量下降及其与Cx43的结构共定位关系增强,则可能是心房颤动时心肌细胞的自我保护、延缓电重构的机制。
目的:探討M3受體及Cx43在心房顫動髮生與維持中的作用及二者之間的相互關繫。方法收集94例風濕性心髒病瓣膜置換術患者右心房組織,按是否存在心房顫動分為心房顫動組( AF組,49例)和竇性心律組( SR組,45例),採用免疫熒光在激光共聚焦顯微鏡下觀察M3受體和Cx43蛋白的錶達及兩者的結構共定位情況,採用Western blot方法檢測兩組M3受體和Cx43蛋白的蛋白錶達量。結果與SR組相比,AF組心房組織M3受體及Cx43蛋白錶達量下降(P<0.05),但M3受體與Cx43的結構共定位關繫增彊(P<0.05)。結論房顫患者右心房組織Cx43錶達量下降,可能是房顫髮生與維持機製之一,M3受體的錶達量下降及其與Cx43的結構共定位關繫增彊,則可能是心房顫動時心肌細胞的自我保護、延緩電重構的機製。
목적:탐토M3수체급Cx43재심방전동발생여유지중적작용급이자지간적상호관계。방법수집94례풍습성심장병판막치환술환자우심방조직,안시부존재심방전동분위심방전동조( AF조,49례)화두성심률조( SR조,45례),채용면역형광재격광공취초현미경하관찰M3수체화Cx43단백적표체급량자적결구공정위정황,채용Western blot방법검측량조M3수체화Cx43단백적단백표체량。결과여SR조상비,AF조심방조직M3수체급Cx43단백표체량하강(P<0.05),단M3수체여Cx43적결구공정위관계증강(P<0.05)。결론방전환자우심방조직Cx43표체량하강,가능시방전발생여유지궤제지일,M3수체적표체량하강급기여Cx43적결구공정위관계증강,칙가능시심방전동시심기세포적자아보호、연완전중구적궤제。
Objective To investigate the potential roles of M 3 receptor and connexin 43 ( Cx43 ) in the occurrence and maintenance of human atrial fibrillation ( AF) and the relationship between them .Methods The right atrial tissues were obtained from 94 patients with rheumatic heart disease undergoing cardiac surgery , and then were divided into group AF (n=49), and sinus rhythm group (group SR, n=45).The co-localization of M3 receptor and Cx43 was detected by immunofluorescence and confocal microscopy .The expression levels of M3 receptor and Cx43 protein were measured by Western blotting.Results Compared with group SR, the expression levels of M3 receptor and Cx43 protein were signifi-cantly down-regulated (P<0.05), while the co-localization of M3 receptor and Cx43 were enhanced in the group AF (P<0.05).Conclusions The down-regulation of Cx43 in the right atrial tissues of AF patients may be one of the mechanisms of occurrence and maintenance of AF , and the decrease of M3's expression and increase of co-localization of M3 receptor and Cx43 may be the protective mechanisms of preventing atrial electrical remodeling produced by cardiomyocytes .