邹游 张雷波 肖昌武 易星 陈始明.不同剂量柚皮素对FADU细胞生长的调节及机制研究[J].,2015,15(15):2824-2828 |
不同剂量柚皮素对FADU细胞生长的调节及机制研究 |
The Influence of Different Concentrations of Naringenin on the Growth ofFADU Cells and its Action Mechanisms |
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DOI: |
中文关键词: 柚皮素 FADU 细胞 作用机制 |
英文关键词: Naringenin FADU cells Mechanism |
基金项目:国家自然科学基金项目(81172569) |
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中文摘要: |
目的:探究不同剂量柚皮素(naringenin)对人下咽癌FADU细胞的作用及其相关机制。方法:以不同剂量(0、100、200、400、
800 ug/mL)柚皮素对FADU细胞进行处理,倒置显微镜观察细胞形态学变化;cck-8 法检测药物作用后不同时间(24、48、72 h)
FADU 细胞增殖的变化;流式细胞仪检测柚皮素作用48 h 细胞凋亡的变化;采用Transwell趋化小室体外侵袭实验测定48 h后细
胞的侵袭能力的变化;蛋白免疫印迹法检测48 h后细胞内PI3K/AKT 信号通路凋亡相关蛋白表达的影响。结果:cck-8 法检测发
现柚皮素抑制FADU 细胞增殖作用明显,呈浓度和时间依赖性;流式细胞结果发现200, 400, 800 ug/mL柚皮素作用48 h后,
FADU 细胞的凋亡率显著增高,差异有统计学意义(P<0.05)。Transwell 体外侵袭实验发现,随着柚皮素浓度增加,FADU细胞穿透
聚碳酸酯滤膜的能力逐渐减弱,柚皮素有效的抑制FADU 细胞在体外的侵袭能力,呈浓度依赖性。同时,蛋白免疫印迹法凋亡相
关蛋白检测结果表明,FADU 细胞内BCL2、P-AKT 和P-PI3K 蛋白表达均受到明显抑制。结论:柚皮素能有效抑制人下咽癌
FADU 细胞的增殖、体外侵袭能力,诱导细胞凋亡;其机制与下调PI3K/AKT 信号通路凋亡相关蛋白表达有关。 |
英文摘要: |
Objective:To explore the influence of different concentrations of naringenin on the growth of hypopharyngeal carcinoma
FADU cells and its action mechanisms.Methods:The role of naringenin on hypopharyngeal carcinoma on the growth of FADU cells was
assessed after treated at the concentrations of 0, 100, 200, 400, 800 ug/ml for 24, 48 and 72 hours. Using the CCK8 method, the effects of
naringenin on the growth of FADU cells was measured after treated in different dose. Using the flow cytometry, the effects of naringenin
on the apoptosis of FADU cells was measured after treated in different dose. Using the transwell method, the effects of naringenin
on the migration ability of FADU cells was measured after treated in different dose. Using the western-blot method, the expression of
BCL2, P-AKT, PI3K was measured.Results:Compared with the control group, cell proliferation rate, migration ability, expression of
BCL2, P-AKT, PI3K decreased with the increase of dose and cell apoptosis rate increases with the dose increased significantly.Conclusion:The naringenin has inhibitory effect on FADU cell growth, migration and induced apoptosis of cells. Its mechanismcould be related
to the reduction of protein expression in PI3K/AKT signal pathways. |
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