摘要
目的探讨P38信号通路在δ氨基酮戊酸(ALA)-光动力疗法(PDT)诱导皮肤鳞状细胞癌细胞株(SCL-1)凋亡中的作用。方法将SCL-1细胞分为空白对照组、ALA组、激光照射组、ALA-PDT组和P38阻断剂ALA-PDT组。Western blot检测各组细胞干预30min,60min,90min后磷酸化P38,Elk-1的表达;Western blot检测P38阻断剂ALA-PDT组细胞多聚(ADP-核糖)聚合酶(PARP)的表达。用MTT法分别检测各组细胞在干预后24h,48h,72h的光密度值,计算各组细胞存活率。用Annexin V-FITC/PI双染流式细胞术检测各组细胞干预后24h,48h,72h细胞的凋亡率。结果磷酸化P38、磷酸化Elk-1在ALA-PDT组细胞表达显著高于其余各组;P38阻断剂ALA-PDT组PARP裂解为85kDa大小的片段增多。与空白对照组、ALA组和激光照射组相比,ALA-PDT组及P38阻断剂ALA-PDT组细胞的存活率显著下降、细胞的凋亡率显著增高。以上差异均有统计学意义。结论 P38通路的激活抑制ALA-PDT诱导的细胞凋亡,阻断这条通路可能成为增强ALA-PDT杀伤皮肤鳞癌细胞新的治疗靶点。
Objective To explore the effect of P38 signaling pathway in killing scl-1 cells induced by 5-aminolevulinic acids-based（ALA） photodynamic therapy （PDT）. Methods SCL-1 cells were divided into control group, ALA group,light group, ALA-PDT group and inhibitor of P38 group. Western blot technique was used to detect the expression of p-P38, p-Elk-1 and PARP （ poly ADP-ribose polymerase） after intervening 30min, 60min,90min of each cell groups. MTF was used to analyzed the cell viability after optical density value of each group were obtained 24h,48, and 72h. Flow cytometry with Annexin V-FITC/PI double staining tech- nique was employed to detect apoptosis of each cell after intervening 24h,48h and 72h. Results The expression of p-P38 and p-Elk-1 were significantly higher in ALA-PDT group than the other groups. PARP of 85KDa was increased significantly in inhibitor of P38 group. Compared with control group, ALA group and light group, cell survival rate of ALA-PDT group and inhibitor of P38 group were decreased significantly, and the apoptosis rate of ALA-PDT group and inhibitor of P38 group were increased remarkably. Conclusion The activation of P38 signaling pathway can inhabit cell apoptosis caused by ALA-PDT. Blocking the pathway may become a new therapeutic target to enhance the treatment of ALA PDT on killing skin squamous cancer cells.
出处
《中国皮肤性病学杂志》
CAS
北大核心
2014年第4期341-345,共5页
The Chinese Journal of Dermatovenereology
基金
国家自然科学基金项目(81060181)
宁夏自然科学基金资助项目(NZ1222)
