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目的:研究吲哚-3-甲醇(I3C)在体内和体外实验中对鼻咽癌细胞的抑制作用及其可能的机制。方法:在体外实验中,以0、100、200、300μmol/L不同浓度的I3C分别作用于人鼻咽癌CNE2细胞株0、24、48和72h后,检测细胞增殖能力。检测各浓度I3C处理CNE2细胞株48h后细胞凋亡率。检测各浓度I3C处理后PI3K/Akt通路相关蛋白PI3Kp110α、PI3Kp85、p-Akt和p-GSK3-β的表达水平。在体内实验中,将BALB/c裸鼠分为I3C预防组、I3C治疗组和对照组。通过给裸鼠种植肿瘤细胞成瘤,预防组和治疗组的裸鼠均给予含0.5%的I3C的饲料喂养,检测各组裸鼠肿瘤生长情况,8周后检测各组裸鼠肿瘤中PI3K/Akt通路相关蛋白的表达水平。结果:随着I3C浓度的增加,细胞的增殖能力明显减弱,凋亡率显著增加,PI3K/Akt通路相关蛋白的表达水平降低。在动物实验中,与对照组相比,8周后预防组和治疗组肿瘤体积明显缩小,裸鼠肿瘤中PI3K/Akt通路相关蛋白的表达水平也降低。同时,苏木精-伊红染色检测各组小鼠心、肝、肾组织未见明显变化。结论:I3C可以在体内和体外有效地抑制鼻咽癌细胞的生长,且诱导凋亡,其作用机制可能是抑制PI3K/Akt信号通路。
Objective: To study the inhibitory effect of indole-3-methanol (I3C) on nasopharyngeal carcinoma cells in vitro and in vivo and its possible mechanism. Methods: In vitro, the proliferation of human nasopharyngeal carcinoma cell line CNE2 was induced by 0, 100, 200, 300μmol / L different concentration of I3C at 0, 24, 48 and 72 hours respectively. The apoptosis rate of CNE2 cells treated with I3C at various concentrations for 48 hours was measured. The expression levels of PI3Kp110α, PI3Kp85, p-Akt and p-GSK3-β in PI3K / Akt pathway after treatment with various concentrations of I3C were detected. In vivo experiments, BALB / c nude mice were divided into I3C prevention group, I3C treatment group and control group. The nude mice in both prophylaxis group and treatment group were fed with 0.5% I3C diet to test the tumor growth of nude mice in each group. After 8 weeks, the tumor growth of PI3K / Akt pathway related protein expression levels. Results: With the increase of I3C concentration, the proliferation of cells was obviously weakened, the apoptosis rate was significantly increased, and the expression of PI3K / Akt pathway related protein was decreased. In animal experiments, compared with the control group, the tumor volume of the preventive group and the treatment group significantly decreased after 8 weeks, and the expression level of the PI3K / Akt pathway-related protein in the nude mice tumor also decreased. At the same time, hematoxylin-eosin staining showed no significant changes in the heart, liver and kidney tissues of mice in each group. CONCLUSION: I3C can effectively inhibit the growth of nasopharyngeal carcinoma cells in vitro and in vivo and induce apoptosis. Its mechanism may be to inhibit the PI3K / Akt signaling pathway.