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目的 探讨全反式维甲酸 (ATRA)抑制视网膜母细胞瘤 (Rb)细胞生长并诱导其凋亡的作用及信号转导机制。方法 应用3 H 胸腺嘧啶掺入分析法观察ATRA对细胞生长的抑制作用 ;用流式细胞仪分析ATRA对Y79细胞周期的影响 ;以DNA片段凝胶电泳分析细胞凋亡 ;用Westernblot分析c jun氨基末端激酶 (JNK)的磷酸化。结果 ATRA可明显抑制Y79细胞的生长 ,1μmol/L处理 36h时 ,3 H 胸腺嘧啶掺入率下降达 4 0 % ,Y79细胞被阻滞于G0 /G1期 ,并出现Sub G1峰。ATRA可诱导Y79细胞凋亡 ,此凋亡过程可被JNK的阻断剂Curcumin阻断 ;在此过程中 ,JNK被激活并磷酸化。结论ATRA可抑制Y79细胞生长并诱导其凋亡 ,其过程是由磷酸化的JNK介导 ,提示ATRA可能是一种潜在的抗Rb化疗药物。
Objective To investigate the effects of all-trans retinoic acid (ATRA) on the growth and apoptosis of retinoblastoma (Rb) cells and its mechanism of signal transduction. Methods 3H-thymidine incorporation assay was used to observe the inhibitory effect of ATRA on cell growth. The effect of ATRA on the cell cycle of Y79 was analyzed by flow cytometry. The apoptosis of Y79 cells was analyzed by DNA fragmentation gel electrophoresis. Phosphorylation of terminal kinase (JNK). Results ATRA could significantly inhibit the growth of Y79 cells. When treated with 1 μmol / L for 36 h, the incorporation of 3 H thymidine decreased 40%, and Y79 cells were arrested in G0 / G1 phase with Sub G1 peak. ATRA induces apoptosis in Y79 cells, which is blocked by Curcumin, a blocker of JNK; during this process, JNK is activated and phosphorylated. Conclusion ATRA can inhibit the growth of Y79 cells and induce its apoptosis. The process is mediated by phosphorylated JNK, suggesting that ATRA may be a potential anti-Rb chemotherapeutic drug.