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目的:探讨表没食子儿茶素没食子酸酯(Epigallocatechin-3-gallate,EGCG)体外抑制潜伏性膜蛋白1转化鼻咽上皮细胞NP69(NP69-LMP1)增殖的机制。方法:采用MTT法检测EGCG抑制NP69-LMP1细胞增殖的IC50值;选用细胞生长曲线、软琼脂集落形成实验和平皿克隆形成实验观察EGCG抑制NP69-LMP1细胞增殖的作用;采用Western-blot检测Wnt1、β-catenin的表达及磷酸化。结果:EGCG抑制NP69-LMP1细胞增殖的IC50值为47.7mg.L-1;EGCG对NP69-LMP1细胞增殖的抑制作用呈浓度和时间依赖性(n=3,P<0.05)。EGCG呈浓度依赖性抑制Wnt1和β-catenin蛋白的表达,促进β-catenin蛋白的磷酸化。结论:EGCG通过降低Wnt1和β-catenin蛋白表达,增加β-catenin蛋白磷酸化水平,发挥对NP69-LMP1细胞增殖的抑制作用。
AIM: To investigate the mechanism of Epigallocatechin-3-gallate (EGCG) inhibiting the proliferation of latent membrane protein-1-transformed nasopharyngeal epithelial cells NP69 (NP69-LMP1) in vitro. Methods: The IC50 of EGCG on the proliferation of NP69-LMP1 cells was detected by MTT assay. The proliferation of NP69-LMP1 cells was detected by cell growth curve, soft agar colony formation assay and plate clone formation assay. The expression of Wnt1, β-catenin expression and phosphorylation. Results: The IC50 value of EGCG on the proliferation of NP69-LMP1 cells was 47.7 mg.L-1. The inhibitory effect of EGCG on the proliferation of NP69-LMP1 cells was concentration-dependent and time-dependent (n = 3, P <0.05). EGCG inhibited Wnt1 and β-catenin protein expression in a concentration-dependent manner, and promoted the phosphorylation of β-catenin protein. CONCLUSION: EGCG can inhibit the proliferation of NP69-LMP1 cells by decreasing the expression of Wnt1 and β-catenin and increasing the phosphorylation of β-catenin.