CAJ | 학술논문

目的：探讨细胞外信号调节激酶（ERK）通路是否参与对人牙髓干细胞（hDPSCs）增殖及分化过程的调控。方法：用不同浓度的ERK通路抑制剂U0126干预hDPSCs，用CCK－8法检测细胞增殖；在矿化液诱导条件下，用不同浓度U0126干预hDPSCs 14 d，茜素红染色观察矿化结节的形成，RT－PCR检测成骨／成牙相关基因ALP、OCN、DSPP及BSP的表达；Western blot检测U0126（25μmol／L）干预后，ERK通路活性的变化。结果：不同浓度的U0126对hDPSCs的增殖能力无显著影响（P＞0．05）；与对照组相比，不同浓度的U0126对矿化结节的形成和成骨／成牙相关基因ALP、OCN、DSPP及BSP的表达均有抑制作用，25μmol／L U0126的抑制作用最明显（P＜0．05）；Western blot结果显示随着时间的延长，p－ERK的表达量逐步增加，在加入25μmol／L U0126后，p－ERK表达量下降（P＜0．05）。结论：ERK信号通路可能不参与对hDPSCs增殖的调控，而在促进hDPSCs成骨／成牙分化过程中起调控作用。
목적：탐토세포외신호조절격매（ERK）통로시부삼여대인아수간세포（hDPSCs）증식급분화과정적조공。방법：용불동농도적ERK통로억제제U0126간예hDPSCs，용CCK－8법검측세포증식；재광화액유도조건하，용불동농도U0126간예hDPSCs 14 d，천소홍염색관찰광화결절적형성，RT－PCR검측성골／성아상관기인ALP、OCN、DSPP급BSP적표체；Western blot검측U0126（25μmol／L）간예후，ERK통로활성적변화。결과：불동농도적U0126대hDPSCs적증식능력무현저영향（P＞0．05）；여대조조상비，불동농도적U0126대광화결절적형성화성골／성아상관기인ALP、OCN、DSPP급BSP적표체균유억제작용，25μmol／L U0126적억제작용최명현（P＜0．05）；Western blot결과현시수착시간적연장，p－ERK적표체량축보증가，재가입25μmol／L U0126후，p－ERK표체량하강（P＜0．05）。결론：ERK신호통로가능불삼여대hDPSCs증식적조공，이재촉진hDPSCs성골／성아분화과정중기조공작용。
AIM:To investigate the function of ERK signaling pathway in the regulation of proliferation and differentiation of human dental pulp stem cells (hDPSCs).METHODS:hDPSCs were treated with different concen-trations of the ERK signaling pathway inhibitor U0126,and the proliferation was measured by CCK-8 method.The mRNA expression of ALP,OCN,DSPP and BSP was determined by RT-PCR.Alizarin red staining was used to detect the mineralized nodules.ERK signaling pathway activation was analyzed by Western blot.RESULTS:ERK inhibitor U0126 had no significant influence on the proliferation of hDPSCs.U0126 inhibited osteogenic differentiation and denti-nogenic differentiation as observed by Alizarin red staining.U0126,especially at 25 μmol/L,down-regulated the ex-pression of ALP,OCN,DSPP and BSP.U0126 at 25 μmol/L significantly inhibited ERK signaling pathway activation. CONCLUSION:ERK signaling pathway is probably not involved in the proliferation of hDPSCs,but plays an impor-tant role in the osteogenic and dentinogenic differentiation of hDPSCs.