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目的:探讨金丝桃苷对眼睑麟状癌细胞(CAE)增殖和侵袭的抑制作用机制。方法:不同浓度金丝桃苷组加入到眼睑麟状癌细胞中,利用溴化3-(4,5-二甲基噻唑-2)-2,5-二苯基四氮唑(MTT)法测定金丝桃苷组对眼睑麟状癌细胞增殖的抑制作用,流式细胞术检测金丝桃苷对眼睑麟状癌细胞的凋亡率,Transwell法检测金丝桃苷对眼睑麟状癌细胞侵袭的抑制作用,采用间接荧光标记法测定细胞内活性氧(ROS)水平的变化;Western blot法检测眼睑麟状癌细胞中Caspase-3、NF-κB和p-NF-κB的表达。结果:与空白对照组比较,随着药物浓度的增加(5、50、100μg/ml),金丝桃苷对眼睑麟状癌细胞生长的抑制率在不断的增加,眼睑麟状癌细胞侵袭能力呈现不断的下降;流式细胞测细胞凋亡结果显示:随着金丝桃苷浓度的增加,眼睑麟状癌细胞的凋亡率在不断增加,呈现剂量依赖性;眼睑麟状癌细胞内活性氧ROS水平随着金丝桃苷的浓度的增加而明显增加;随着金丝桃苷浓度的增加,凋亡蛋白Caspase-3和NF-κB的表达呈不断的增加,p-NF-κB的表达呈现不断的减少。结论:金丝桃苷通过Caspase-3级联凋亡途径、NF-κB因子调控途径和提升ROS水平的共同诱导了眼睑麟状癌细胞凋亡。
Objective: To investigate the inhibitory mechanism of hyperoside on the proliferation and invasion of eyelid carcinoma cells (CAE). Methods: The hyperoside groups were added to the eyelid cancer cells, and the cells were treated with 3- (4,5-dimethylthiazol-2) -2,5-diphenyltetrazolium bromide (MTT) The inhibitory effect of hyperoside on the proliferation of eyelid carcinoma cells was determined. The apoptosis rate of hypericin on eyelid carcinoma cells was detected by flow cytometry. The influence of hyperoside to the eyelid carcinoma cells The expression of Caspase-3, NF-κB and p-NF-κB in eyelid carcinoma cells was detected by Western blot. The changes of intracellular reactive oxygen species (ROS) were measured by indirect fluorescent labeling. RESULTS: Compared with the blank control group, the inhibitory rate of hyperoside on the growth of eyelid carcinoma cells was continuously increased with the increase of drug concentration (5, 50 and 100 μg / ml), and the invasive ability of eyelid carcinoma cells Flow cytometry results showed that the apoptosis rate of eyelid carcinoma cells increased with the increase of hyperoside concentration in a dose-dependent manner. The intraocular activity of eyelid carcinoma cells The level of ROS increased with the increase of concentration of hyperoside. The expression of Caspase-3 and NF-κB increased with the increase of concentration of hyperoside. The expression of p-NF-κB Expression showed a continuous decrease. CONCLUSION: Hyperin induces the apoptosis of eyelid carcinoma cells through Caspase-3 cascade, NF-κB pathway and ROS enhancement.