摘要
目的探讨芬太尼对人胃癌细胞SGC-7901增殖影响及机制研究。方法以0(对照组)、0.5、5、50 nmol/L芬太尼作用胃癌细胞SGC-7901一定时间,MTT法检测芬太尼对SGC-7901细胞活力的影响;流式细胞术检测芬太尼对SGC-7901细胞周期的影响;Western blot检测细胞凋亡相关蛋白cyclin D1,Bcl-2的表达。结果与对照组比较,0.5,5,50 nmol/L芬太尼可显著抑制细胞的活力,在48 h抑制程度最高。0.5,5,50 nmol/L芬太尼使细胞周期阻滞在G1期,与对照组相比,随着给药浓度的增加,芬太尼能显著抑制cyclin D1,Bcl-2的表达(P<0.05)。结论芬太尼可抑制胃癌SGC-7901细胞增殖。
Objective To explore mechnism and effect of fentanyl on proliferation of gastric cancer SGC-7901 cell. Methods Gastric cancer SGC-7901 cell was cultured with fentanyl of 0（ negative control）,0. 5,5 and 50 nmol / L,MTT method was used to detect the effect of fentanyl on SGC-7901 viability. The effect of fentanyl on SGC-7901 cell cycle was measured by flow cytometry. The level of cell related protein,cell cycle protein cyclin D1,Bcl-2. Results Compared with control group,fentanyl（ 0. 5,5,50 nmol / L） could inhibit SGC-7901 cell viability,and the inhibitory rate was highest at48 h. 0. 5,5,50 nmol / L fentanyl made cell cycle arrested in G1 phase. Compared with control group,fentanyl can significantly inhibit cyclin D1 and Bcl-2 expression with drug concentration increasing（ P〈0. 05）. Conclusion These results suggeste fentanyl inhibit proliferation of gastric cancer SGC-7901 cell.
出处
《中国生化药物杂志》
CAS
2015年第9期38-40,共3页
Chinese Journal of Biochemical Pharmaceutics
基金
中国肝炎防治基金会天晴肝病研究基金(TQGB20120013)
