摘要
目的探讨熊果酸(ursolic acid,UA)对人食管癌KYSE105细胞增殖、细胞凋亡的影响及其分子机制。方法应用0~50μmol/L熊果酸处理KYSE105细胞24~72h后,采用四甲基偶氮唑蓝法(MTT)检测细胞增殖抑制率;流式细胞术(FCM)检测KYSE105细胞周期及凋亡率;RT-PCR检测B细胞淋巴瘤/白血病-2(Bcelllymphoma/lewkmia-2,bcl-2)、Bcl-2相关X蛋白(Bcl-2as-sociated X protein,bax)及细胞周期素D1(cyclinD1)mRNA的表达。结果熊果酸作用后KYSE105细胞生长明显减慢,抑制率8.55%~89.48%(P<0.05),呈时间-剂量效应关系,使细胞周期阻滞在G0/G1期,凋亡率16.62%~21.54%(P<0.05)。baxmR-NA表达升高,bcl-2、cyclinD1mRNA表达下调(P<0.05)。结论熊果酸能明显抑制KYSE105细胞的增殖,诱导其凋亡,其机制可能与抑制bcl-2、cyclinD1表达,同时促进bax表达有关。
Objective To explore the effects of ursolic acid (UA) on proliferation,apoptosis of KYSE105 cells in esophageal carcinoma and possible mechanism.Methods The KYSE105 cells were treated with 0~50 μmol/L curcumin for 24~72 h,then the inhibition ratio of cell proliferation was detected by MTT.The cell cycle and apoptosis rate were detected by flow cytometry.The expression levels of bcl-2,bax and cyclinD1 mRNA were detected by RT-PCR.Results After UA treatment,the growth of KYSE105 cells was significantly inhibited in a time-dose dependent manner:the inhibition rates were 8.55%~89.48% (P〈0.05),the cell cycle was arrested in G0/G1 phase,and the apoptosis rates were 16.62%~21.54% (P〈0.05).The expression level of bax mRNA increased while the expression levels of bcl-2,cyclinD1 decreased obviously (P〈0.05).Conclusion UA shows obvious inhibitory effects on KYSE105 cells.The effects may be related to induce apoptosis and arrest cell cycle.The mechanism may be associated with upregulating bax and downregulating bcl-2,cyclinD1.
出处
《胃肠病学和肝病学杂志》
CAS
2010年第2期130-133,共4页
Chinese Journal of Gastroenterology and Hepatology