中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2012年
5期
888-890
,共3页
Cajal间质细胞%干细胞因子%c-kit%胃肠动力
Cajal間質細胞%榦細胞因子%c-kit%胃腸動力
Cajal간질세포%간세포인자%c-kit%위장동력
Interstitial cells of Cajal%Stem cell factor%c-Kit%Gastrointestinal motility
目的 观察阻断c-Kit信号通路致Caja1间质细胞(ICC)缺失,而c-Kit的配体干细胞因子(SCF)能否促进其恢复.方法 将新出生的小鼠于腹腔内隔天注射c -Kit抗体(ACK2) 100μg,共5次,建立ICC缺失模型,再于第10天腹腔内注射SCF,连续注射5d后观察空肠电节律并通过免疫组织化学法观察Cajal间质细胞的恢复；采用逆转录-聚合酶链反应(RT-PCR)、Western blot法检测c-Kit基因转录和表达.结果 当c-Kit受体被阻断后,空肠ICC几乎缺失且慢波消失；SCF腹腔注射给药可使ICC缺失小鼠空肠慢波频率明显增快(7.83±1.34)次/min(P ＜0.01),振幅也有加大(0.044±0.009) mV(P ＜0.05)；而且肌间神经丛区ICC增多,c-Kit mRNA及c-Kit蛋白表达也上调.结论 c-Kit与其配体SCF结合所启动的信号途径对ICC的生存及表型维持至关重要.阻断c-Kit的作用后,ICC会出现缺失.通过给予外源性SCF刺激后,缺失的ICC部分恢复,且这种恢复与c-Kit表达水平的上调有关.
目的 觀察阻斷c-Kit信號通路緻Caja1間質細胞(ICC)缺失,而c-Kit的配體榦細胞因子(SCF)能否促進其恢複.方法 將新齣生的小鼠于腹腔內隔天註射c -Kit抗體(ACK2) 100μg,共5次,建立ICC缺失模型,再于第10天腹腔內註射SCF,連續註射5d後觀察空腸電節律併通過免疫組織化學法觀察Cajal間質細胞的恢複；採用逆轉錄-聚閤酶鏈反應(RT-PCR)、Western blot法檢測c-Kit基因轉錄和錶達.結果 噹c-Kit受體被阻斷後,空腸ICC幾乎缺失且慢波消失；SCF腹腔註射給藥可使ICC缺失小鼠空腸慢波頻率明顯增快(7.83±1.34)次/min(P ＜0.01),振幅也有加大(0.044±0.009) mV(P ＜0.05)；而且肌間神經叢區ICC增多,c-Kit mRNA及c-Kit蛋白錶達也上調.結論 c-Kit與其配體SCF結閤所啟動的信號途徑對ICC的生存及錶型維持至關重要.阻斷c-Kit的作用後,ICC會齣現缺失.通過給予外源性SCF刺激後,缺失的ICC部分恢複,且這種恢複與c-Kit錶達水平的上調有關.
목적 관찰조단c-Kit신호통로치Caja1간질세포(ICC)결실,이c-Kit적배체간세포인자(SCF)능부촉진기회복.방법 장신출생적소서우복강내격천주사c -Kit항체(ACK2) 100μg,공5차,건립ICC결실모형,재우제10천복강내주사SCF,련속주사5d후관찰공장전절률병통과면역조직화학법관찰Cajal간질세포적회복；채용역전록-취합매련반응(RT-PCR)、Western blot법검측c-Kit기인전록화표체.결과 당c-Kit수체피조단후,공장ICC궤호결실차만파소실；SCF복강주사급약가사ICC결실소서공장만파빈솔명현증쾌(7.83±1.34)차/min(P ＜0.01),진폭야유가대(0.044±0.009) mV(P ＜0.05)；이차기간신경총구ICC증다,c-Kit mRNA급c-Kit단백표체야상조.결론 c-Kit여기배체SCF결합소계동적신호도경대ICC적생존급표형유지지관중요.조단c-Kit적작용후,ICC회출현결실.통과급여외원성SCF자격후,결실적ICC부분회복,차저충회복여c-Kit표체수평적상조유관.
Objective To observe interstitial cells of Cajal (ICC) loss by blocking the c-Kit receptors and determine whether exogenous stem cell factor (SCF) can promote ICC restoration following the blockade of c-Kit signaling.Methods New-born mice were injected intraperitoneally with antibody of c-Kit (ACK2 ),100 μg every two days for 5 times.Secondly,the mice with ICC loss were injected intraperitoneally with SCF for 5 days continuously,and control groups were given saline.The activities of slow waves,the distribution of ICC,and the mRNA and protein expression of c-Kit were determined in the jejunum.Results When c-Kit receptors were blocked,ICC nearly disappeared from the jejunum accompanied by the loss of electrical slow waves.After intraperitoneal injection of SCF,the amplitude of slow waves in ICC loss mice was restored to ( 0.044 ± 0.009 ) mV ( P ＜ 0.05 ),whereas the frequency recovered to ( 7.83 ±1.34)/min (P ＜ 0.01 ).Furthermore,labeling for c-Kit+ cells in the myenteric plexus was increased,and c-Kit mRNA and protein expression was up-regulated compared to that of controls.Conclusion The cell signaling via c-Kit and its ligand SCF is the critical pathway associated with the control of ICC survival and maintenance.The restoration of ICC number and jejunal electrical rhythm,resulting from blockade of the c-Kit signaling pathway,could be promoted by exogenous SCF administration.
