摘要
目的:研究植酸对肝癌HepG2细胞的生长抑制作用并探讨其机制。方法:将含不同浓度(0、1、2和3mmol/L)植酸的培养液作用于体外培养的HepG2细胞,应用免疫细胞化学法检测HepG2细胞内增殖细胞核抗原(PCNA)的表达;RT-PCR法检测细胞癌基因Mdm2mRNA的表达;蛋白质印迹法检测核转录因子NF-кB p65的表达变化。结果:1、2和3mmol/L植酸作用组PCNA蛋白表达的A值分别为0.189±0.004、0.179±0.003和0.175±0.002,0mmol/L组即对照组为0.209±0.013,植酸作用组低于对照组,差异有统计学意义,F=21.491,P<0.05;Mdm2mRNA的表达值分别为0.871±0.058、0.720±0.035和0.593±0.061,对照组为0.889±0.092,植酸作用组低于对照组,差异有统计学意义,F=13.698,P<0.05;NF-кB p65蛋白表达值分别为0.933±0.007、0.920±0.014和0.908±0.012,对照组为0.965±0.021,植酸作用组低于对照组,差异有统计学意义,F=8.472,P<0.05。结论:植酸具有抑制肝癌HepG2细胞生长的作用,其机制可能与植酸下调PCNA、Mdm2、NF-кB p65的表达从而起到抑制HepG2细胞的增殖和诱导凋亡有关。
OBJECTIVE：To study the growth inhibition and mechanism of phytic acid on HepG2 cells. METHODS： HepG2 cells were cultured in vitro and treated with various concentrations （0,1,2,3 mmol/L）of phytic acid. Immunocyto- chemical stain was used to detect the expression of PCNA. RT-PCR was used to determine the expression of oncogene Mdm2 mRNA in HepG2 cells. Western Blot was used to detect the expression of nuclear transcription factor NF-KB p65. RESULTS：The OD values of PCNA expression in phytic acid groups （1,2,3 mmol/L） were 0. 189±0. 004,0. 179 ± 0. 003,0. 175±0. 002 and in the control group （0 mmol/L） it was 0. 209±0. 013. The expression in phytic acid groups was lower than that in the control group, and the difference was statistically significant（F= 21. 491, P〈0.05）. Mdm2 mRNA expression values in phytic acid groups were 0. 871±0. 058,0. 720±0. 035,0. 593±0. 061 and that in the control group was 0. 889±0. 092, the expression value in phytic acid groups were lower than that in the control group and the difference was statistically significant（F= 13. 698,P〈0.05）. NF-KB p65 protein expression values in phytic acid groups were 0. 933±0. 007,0. 920±0. 014,0. 908±0. 012,in control group it was 0. 965±0. 021,and the expression level in phytic acid groups were lower than that in control group and the difference was statistically significant（F= 8. 472, P〈0.05）. CONCLUSION.. Phytic acid inhibits the growth of HepG2 cells. The mechanism may be related to the decrease ex- pression of PCNA, Mdm2, NF-KB p65 with phytic acid, as well as the inhibition of proliferation and induction of apoptosis on HepG2 cells.
出处
《中华肿瘤防治杂志》
CAS
北大核心
2013年第13期982-985,共4页
Chinese Journal of Cancer Prevention and Treatment
基金
山东省博士基金(2007BS03042)
