摘要
目的:探讨阿司匹林对人牙髓干细胞(h DPSCs)在体外增殖及分化过程的作用。方法:取体外培养的h DPSCs,加入矿化液和0.005、0.05、0.5、5 mmol/L的阿司匹林为实验组;单独加矿化液为对照组;不加矿化液为空白组。MTT法检测细胞增殖;在矿化液条件下阿司匹林诱导14 d时,茜素红染色观察细胞矿化情况,用western blot检测MAPK信号通路在h DPSCs分化中的作用。结果:0.05、0.005 mmol/L的阿司匹林均可促进h DPSCs增殖,5 mmol/L的阿司匹林则明显抑制h DPSCs的增殖;0.5、0.05 mmol/L的阿司匹林可抑制h DPSCs矿化结节的形成。Western blot结果显示,0.5 mmol/L阿司匹林刺激可抑制p-p38、p-JNK的表达且与作用时间相关,而对p-ERK表达无明显影响。结论:阿司匹林对h DPSCs的作用有剂量依赖性。阿司匹林可能是通过抑制MAPK的p38、JNK信号通路而抑制h DPSCs成牙向分化。
AIM: To investigate the effects of aspirin on the proliferation and differentiation of dental pulp stem cells( h DPSCs). METHODS: h DPSCs were cuture in mineralization induction medium and treated with different concentrations of aspirin for different periods respectively. The proliferation of h DPSCs was examined by MTT assay.The mineralization of the cells was observed by alizarin red staining after aspirin treatment for 14 days. MAPK expression of the cells was detected by Western blot. RESULTS: Aspirin at 0. 005 and 0. 05 mmol / L promoted the prolifereation of h DPSCs,at 0. 5 mmol / L showed a decreased stimulating effect. 5 mmol / L aspirin inhibited the cell prolifereation. Aspirin at 0. 5 and 0. 05 mmol / L reduced the formation of mineralized nodules. 0. 5 mmol / L aspirin time-dependantly decreased JNK and p38 expression while it showed no significant influence on ERK1 /2 expression. CONCLUSION: Aspirin may inhibits odontogenic differentiation of h DPSCs through inhibiting p38 and JNK MAPK signaling pathway.
出处
《牙体牙髓牙周病学杂志》
CAS
2016年第4期213-217,共5页
Chinese Journal of Conservative Dentistry
基金
国家自然科学基金(81271125)