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[目的]探讨蜂胶黄酮pinobanksin-3-acetate对体外培养的胃癌SGC-7901细胞增殖、凋亡及部分基因表达的影响。[方法]采用四甲基偶氮唑盐(MTT)显色法检测不同浓度PB3A作用不同时间对SGC-7901细胞生长所产生的影响,计算生长抑制率和IC50值;倒置显微镜观察PB3A干预后细胞的形态变化;AnnexinⅤ-FITC/PI双染色、流式细胞仪检测细胞凋亡率;Western blot法检测PB3A(40、80μg/ml)干预24h后SGC-7901细胞FOS、GEM、RGS2、GADD45G及HSPA6的蛋白表达水平,利用Spearman进行候选基因相关性分析。[结果 ]PB3A可明显抑制SGC-7901细胞的增殖(P<0.05),且抑制作用呈时间和剂量依赖性。随PB3A剂量的增多,SGC-7901细胞的凋亡率渐增,细胞的早期凋亡率从25.6%提高到50.2%。通过40μg/ml和80μg/ml PB3A干预胃癌SGC-7901细胞24h后与对照组相比,高浓度组GADD45G、HSPA6、GEM、RGSR及FOS蛋白表达有极显著性差异(P<0.01),而低浓度组GADD45G、GEM和HSPA6蛋白表达有显著性差异(P<0.05)。[结论 ]PB3A在体外可明显抑制胃癌SGC-7901细胞增殖并诱导凋亡的作用,并呈剂量依赖性变化趋势。机制可能与其诱导GEM、RGSR、FOS及HSPA6蛋白的上调表达有关,以上基因可能相互协同导致肿瘤细胞增殖信号通路的抑制并促进胃癌细胞的凋亡。
[Objective] To investigate the effects of propolis flavone pinobanksin-3-acetate on proliferation, apoptosis and partial gene expression of gastric cancer SGC-7901 cells in vitro. [Method] MTT assay was used to detect the effects of different concentrations of PB3A on the growth of SGC-7901 cells at different times, and the growth inhibition rates and IC50 values were calculated. The cells were treated with PB3A The apoptosis of SGC-7901 cells was detected by AnnexinⅤ-FITC / PI double staining and flow cytometry. The expression of FOS, GEM, RGS2, GADD45G and HSPA6 in SGC-7901 cells treated with PB3A Of the protein expression level, using Spearman candidate gene correlation analysis. [Result] PB3A could significantly inhibit the proliferation of SGC-7901 cells (P <0.05), and the inhibitory effect was time-and dose-dependent. With the increase of PB3A dose, the apoptosis rate of SGC-7901 cells gradually increased, and the early apoptosis rate increased from 25.6% to 50.2%. Compared with the control group, the expression of GADD45G, HSPA6, GEM, RGSR and FOS in gastric cancer SGC-7901 cells treated with 40μg / ml and 80μg / ml PB3A for 24h were significantly different (P <0.01) The concentration of GADD45G, GEM and HSPA6 protein expression was significantly different (P <0.05). [Conclusion] PB3A can significantly inhibit the proliferation and induce apoptosis of gastric cancer SGC-7901 cells in vitro and in a dose-dependent manner. The mechanism may be related to its up-regulation of GEM, RGSR, FOS and HSPA6 protein expression, the above genes may cooperate with each other to lead to the inhibition of tumor cell proliferation signaling pathway and promote gastric cancer cell apoptosis.