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目的研究白藜芦醇(resveratrol,Res)抑制人结肠癌细胞生长的作用与p38 MAPK的可能关系。方法利用结晶紫染色、Western blot和流式细胞术检测Res对LoVo细胞增殖的抑制作用;Western blot分析Res对LoVo细胞凋亡的促进作用,以及Res对p38 MAPK磷酸化的影响;利用p38MAPK抑制剂,通过结晶紫染色和Western blot实验,分析Res抑制结肠癌LoVo细胞增殖的作用与p38 MAPK之间的关系。结果与对照组相比,Res在20μmol·L~(-1)时就能明显抑制LoVo细胞增殖(P<0.05),并促使细胞周期阻滞在S期,上调PCNA蛋白水平;Res能呈浓度依赖性增加Bad的蛋白水平,而抑制Bcl-2蛋白表达;Res对p38 MAPK总蛋白水平无明显影响,但可明显增加p38 MAPK的磷酸化水平;抑制p38 MAPK明显促进LoVo细胞增殖,并能减弱Res对LoVo细胞增殖的抑制作用、对Bad表达促进作用和对Bcl-2表达的抑制作用。结论 Res对LoVo细胞的增殖具有抑制作用并促进凋亡,其机制可能与Res促进p38 MAPK的磷酸化有关。
Objective To study the possible relationship between resveratrol (Res) inhibition of human colon cancer cell growth and p38 MAPK. Methods The inhibitory effect of Res on the proliferation of LoVo cells was detected by crystal violet staining, Western blot and flow cytometry. The effect of Res on the apoptosis of LoVo cells induced by Res and the effect of Res on the phosphorylation of p38 MAPK were analyzed by Western blot. The p38 MAPK inhibitor , The crystal violet staining and Western blot experiments Res analysis of inhibition of colon cancer LoVo cell proliferation and p38 MAPK relationship. Results Compared with the control group, Res significantly inhibited the proliferation of LoVo cells at 20μmol·L -1 (P <0.05), and promoted the cell cycle arrest in S phase and upregulated the expression of PCNA protein. Dependently increased the protein level of Bad and inhibited the expression of Bcl-2 protein. Res had no significant effect on the total protein level of p38 MAPK, but significantly increased the phosphorylation level of p38 MAPK. Inhibition of p38 MAPK promoted the proliferation of LoVo cells and decreased Res on LoVo cell proliferation inhibition, the promotion of Bad expression and inhibition of Bcl-2 expression. Conclusion Res can inhibit the proliferation of LoVo cells and promote apoptosis. The mechanism may be related to the promotion of p38 MAPK phosphorylation by Res.