小分子化合物S1诱导B16细胞凋亡及其机制的研究

The research of mechanism that micromolecule compound S1 induce B16 cell apoptosis

目的探讨小分子化合物S1诱导小鼠黑色素瘤B16细胞凋亡的机制,为S1治疗皮肤黑色素瘤提供理论与实验基础。方法小鼠黑色素瘤B16细胞被分为四组,对照组(Control)、S1低剂量组(S1 2.5μM)、S1中剂量组(S1 5μM)和S1高剂量组(S1 10μM),利用MTT方法检测B16细胞存活率、流式细胞术检测细胞凋亡率、Westernblotting检测凋亡相关蛋白表达水平的变化。结果相对于对照组,小分子化合物S1可以明显降低B16细胞存活率,差异有统计学意义(P<0.05);流式细胞术结果显示,S1可以引起B16细胞凋亡率明显上升同时凋亡相关分子caspase-3表达水平明显升高;与对照组相比,线粒体凋亡相关蛋白Cytochrome C表达水平也出现了明显的升高,差异有统计学意义(P<0.05)。结论小分子化合物S1可能通过线粒体凋亡信号通路引起黑色素瘤细胞发生凋亡。

Objective Explore the apoptosis mechanism of small molecule S1 on B16 cells and improve the therapeutic effect of S1.Methods B16 cells were divided into four groups,control group,S1 2.5 μM group,S1 5 μM group and S1 10 μM group respectively.The survival rate of B16 cells was determined by MTT.The apoptosis rate of B16 cells was determined by Flow cytometry analysis.The apoptosis relative proteins were determined by Western blotting.Results Compared with control group,S1 can decrease the survival rate of B16 cells（P〈0.05）.Small molecule S1 can increase the apoptosis rate of B16 cells significantly.The results of Western Blotting showed that the apoptosis-relative protein cleaved caspase-3 and mitochondrial apoptosis-relative protein Cytochrome C were increased significantly（P〈0.05）.Conclusion Small molecule S1 maybe induce B16 cells apoptosis through mitochondrial apoptosis pathways.