中华临床医师杂志（电子版）
中華臨床醫師雜誌（電子版）
중화림상의사잡지（전자판）
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2013年
13期
5980-5983
,共4页
袁凤来%李霞%金成%姜东林%何庆龙%苏强
袁鳳來%李霞%金成%薑東林%何慶龍%囌彊
원봉래%리하%금성%강동림%하경룡%소강
关节炎,实验性%离子通道%软骨,关节%显微镜检查,共焦%钙离子
關節炎,實驗性%離子通道%軟骨,關節%顯微鏡檢查,共焦%鈣離子
관절염,실험성%리자통도%연골,관절%현미경검사,공초%개리자
Arthritis,experimental%Ion channels%Cartilage,articular%Microscopy,confocal%Ca2+
目的：探讨酸敏感离子通道（ASICs）与酸诱导的大鼠佐剂性关节炎（AA）关节软骨细胞Ca2＋运动的关系。方法雄性SD大鼠12只，分为正常组（ n＝6）和AA模型组（ n＝6）。模型组大鼠制备AA模型，体外培养AA关节软骨细胞，应用Ca2＋荧光指示剂Fluo-3/AM孵育培养的细胞，激光共聚焦显微镜检测有、无细胞外液以及PCTX对细胞外pH 6.0酸作用所致AA关节软骨细胞内Ca2＋荧光强度动态及Ca2＋浓度（[ Ca2＋] i ）变化。结果在无细胞外钙环境中，酸未引起AA关节软骨细胞Ca2＋变化，平均荧光值为45.63±16.38。而在胞外液有Ca2＋的情况下，pH 6.0可引起AA关节软骨细胞Ca2＋短暂性升高（149.56±25.39），与无钙组比较明显增加（P＜0.01）；PCTX对pH 6.0诱导AA关节软骨细胞Ca2＋内流明显抑制作用（60.85±28.73，P＜0.01）。结论 ASICs参与酸诱导的经AA关节软骨细胞Ca2＋内流，可能与关节软骨破坏有关。
目的：探討痠敏感離子通道（ASICs）與痠誘導的大鼠佐劑性關節炎（AA）關節軟骨細胞Ca2＋運動的關繫。方法雄性SD大鼠12隻，分為正常組（ n＝6）和AA模型組（ n＝6）。模型組大鼠製備AA模型，體外培養AA關節軟骨細胞，應用Ca2＋熒光指示劑Fluo-3/AM孵育培養的細胞，激光共聚焦顯微鏡檢測有、無細胞外液以及PCTX對細胞外pH 6.0痠作用所緻AA關節軟骨細胞內Ca2＋熒光彊度動態及Ca2＋濃度（[ Ca2＋] i ）變化。結果在無細胞外鈣環境中，痠未引起AA關節軟骨細胞Ca2＋變化，平均熒光值為45.63±16.38。而在胞外液有Ca2＋的情況下，pH 6.0可引起AA關節軟骨細胞Ca2＋短暫性升高（149.56±25.39），與無鈣組比較明顯增加（P＜0.01）；PCTX對pH 6.0誘導AA關節軟骨細胞Ca2＋內流明顯抑製作用（60.85±28.73，P＜0.01）。結論 ASICs參與痠誘導的經AA關節軟骨細胞Ca2＋內流，可能與關節軟骨破壞有關。
목적：탐토산민감리자통도（ASICs）여산유도적대서좌제성관절염（AA）관절연골세포Ca2＋운동적관계。방법웅성SD대서12지，분위정상조（ n＝6）화AA모형조（ n＝6）。모형조대서제비AA모형，체외배양AA관절연골세포，응용Ca2＋형광지시제Fluo-3/AM부육배양적세포，격광공취초현미경검측유、무세포외액이급PCTX대세포외pH 6.0산작용소치AA관절연골세포내Ca2＋형광강도동태급Ca2＋농도（[ Ca2＋] i ）변화。결과재무세포외개배경중，산미인기AA관절연골세포Ca2＋변화，평균형광치위45.63±16.38。이재포외액유Ca2＋적정황하，pH 6.0가인기AA관절연골세포Ca2＋단잠성승고（149.56±25.39），여무개조비교명현증가（P＜0.01）；PCTX대pH 6.0유도AA관절연골세포Ca2＋내류명현억제작용（60.85±28.73，P＜0.01）。결론 ASICs삼여산유도적경AA관절연골세포Ca2＋내류，가능여관절연골파배유관。
Objective To investigate the relationship between acid sensing ion channels and Ca 2+movement induced by pH 6.0 in articular chondrocytes in rats with adjuvant arthritis .Methods Twelve male SD rats were used for these studies .The rats were divided at random into normal group ( n=6) and AA model group ( n=6).Adjuvant arthritis was induced in rats in AA model group and articular chondrocytes obtained from AA rats were cultured in vitro.The cultured AA articular chondrocytes were in cubated with the calcium ion-sensitive fluorescent indicator fluo-3/AM, and then using the Laser Scanning Confocal Microscopy technique recording intracellular calcium([Ca2+]i) in chondrocytes caused by pH 6.0 or PCTX when cells were immersed in the buffer with or without Ca2+.Results Our results as following,the rapid decreased in extracellular pH 6.0 with Ca2+-free buffer was not found to induce a conspicuous increase in [Ca2+]i in articular chondrocytes of AA rats.Increased Ca2+intensity was 45.63 ±16.38 .The rapid decrease in extracellular pH 6.0 with Ca2+-containing buffer was found to induce a conspicuous increase in [ Ca2+]i in articular chondrocytes of AA rats, increased Ca2+ intensity was 149.56 ±25.39(P<0.01).PCTX almost completely blocked the [Ca2+]i increase observed at low pH in AA rat articular chondrocytes ,increased Ca 2+intensity was 60.85 ±28.73 ( P<0.01 ) .Conclusion ASICs medites acid-induced acid-induced increase in intracellular calcium in rat articular chondrocytes and it may be related with breakdown of articular cartilage .
