摘要
目的观察脱乙酰化酶抑制剂丁酸钠对人胃癌MKN-28细胞增殖的抑制作用,并探讨其作用机制。方法MTT法观察丁酸钠对人胃癌MKN-28细胞的生长抑制作用;流式细胞术检测细胞凋亡及细胞周期;RT-PCR检测丁酸钠作用前后p21WAF1 mRNA的表达。结果1.0、2.5、5.0 mmol/L丁酸钠作用24、48、72 h均可抑制MKN-28细胞增殖,其效果具有时间、剂量依赖性(P<0.05);丁酸钠1.0、2.5、5.0 mmol/L处理72 h后,MKN-28细胞G0/G1期细胞数量显著增加,S期细胞数量显著降低(P<0.05);细胞凋亡率分别为13.7%±0.8%、20.8%±2.4%、33.6%±2.6%,与对照组2.8%±0.4%相比P均<0.05;与对照组比较,丁酸钠处理后p21WAF1转录水平上调。结论丁酸钠可显著抑制人胃癌MKN-28细胞的生长,其可能的机制是通过上调p21WAF1基因的表达,诱导细胞凋亡,使细胞周期阻滞于G0/G1期。
Objective To investigate the effects and mechanism of histone deacetylase inhibitors sodium butyrate on cell growth inhibition in human gastric carcinoma cell MKN-28. Methods The inhibiting effects of cell growth was assayed by MTT method;cell cycles and apoptosis were analyzed by flow cytometry（FCM） ;The expression of apoptosis-related gene p21WAF1 Was detected by RT-PCR before and after sodium butyrate treateded. Results Sodium butyrate （ 1.0,2.5,5.0 retool/L） all showed inhibitory effects on the proliferation of MKN-28cell in dose- and-time dependent manner（ P 〈0.05 ） ; The increasing G0/G1 stage cells and decreasing S phase cells were observed significantly at 72 h after NaB（ 1.0,2.5,5.0 mmol/L） treatment （ P 〈 0. 05 ）, ap6ptosis rates were 13.7% ± 0.8%, 20.8% ± 2.4%, 33.6% ± 2.6% respectively, the difference is significantly when compare with the control groupe 2.8% ± 0.4% （ P 〈 0.05 ）. The level of p21WAF1 was higher in the sodium butyrate treated cell than the cell without treatment. Conclusion Sodium butyrate could inhibit growth of MKN-28 cells effectively. It may be related to p21WAFI gene up-regulating, apoptosis inducing and G0/Gl blocking.
出处
《山东医药》
CAS
北大核心
2009年第38期21-23,共3页
Shandong Medical Journal
基金
江苏省医学重点人才基金资助项目(RC2007076)
