摘要
目的:探究麻醉药丙泊酚对人胃癌SGC-7901细胞体外增殖、凋亡的影响及其作用机制。方法:体外培养人胃癌SGC-7901细胞,分别使用不同浓度(0,2,4,6μg·ml^(-1))的丙泊酚干预SGC-7901细胞(其中0μg·ml^(-1)为对照组),采用克隆形成实验测定丙泊酚对SGC-7901细胞克隆形成能力的影响,噻唑蓝(MTT)法检测丙泊酚对SGC-7901细胞活力的影响,流式细胞仪检测细胞凋亡情况,蛋白免疫印迹(Western blot)法检测增殖细胞核抗原、凋亡相关蛋白以及Wnt/β-连环蛋白(Wnt/β-catenin)信号转导途径相关蛋白水平。在4μg·ml^(-1)的丙泊酚处理的SGC-7901细胞组施加Wnt/β-catenin信号转导途径特异性激活剂氯化锂(Li Cl),检测对SGC-7901细胞增殖和凋亡的影响。结果:与对照组比较,丙泊酚组SGC-7901细胞克隆形成数目、光密度(OD)值、增殖细胞核抗原(PCNA)和Ki-67、β-连环蛋白(β-catenin)、c-myc和细胞周期蛋白D1(cyclin D1)蛋白水平明显降低(P<0.05或P<0.01),凋亡率、Bcl-2相关X蛋白(Bax)和剪切的含半胱氨酸的天冬氨酸蛋白水解酶3(cleaved caspase-3)蛋白水平明显升高(P<0.01)。而Wnt/β-catenin激活剂LiCl可减弱丙泊酚对SGC-7901细胞的增殖抑制的作用,部分逆转丙泊酚对SGC-7901细胞凋亡诱导的作用。结论:丙泊酚抑制人胃癌SGC-7901细胞增殖,促进细胞凋亡,其潜在分子机制是通过抑制Wnt/β-catenin信号转导途径来实现的。
Objective: To explore the effect of anesthetic drug propofol on the proliferation and apoptosis of human gastric cancer SGC-7901 cells in vitro and the underlying mechanism. Methods: Human gastric cancer SGC-7901 cells were cultured in vitro,and different concentrations( 0,2,4 and 6 μg·ml^(-1)) of propofol were used to intervene SGC-7901 cells( 0 μg·ml^(-1) was for the control group). The clone formation experiment was used to determine the effect of propofol on SGC-7901 cell clone formation. MTT was used to detect the effect of propofol on the viability of SGC-7901 cells. Flow cytometry was used to detect the cell apoptosis. Western blot method was used to detect the levels of proliferating cell nuclear antigen,apoptosis-related protein and Wnt/β-catenin signal transduction pathway related proteins. Li Cl,a specific activator of Wnt/β-catenin signal transduction pathway,was applied to the SGC-7901 cell group treated with 4 μg·ml^(-1) propofol,and the proliferation and apoptosis of SGC-7901 cells were detected. Results: Compared with those in the control group,SGC-7901 cell clone formation number,optical density( OD) value,proliferating cell nuclear antigen( PCNA) and Ki-67,β-catenin( β-catenin),c-myc and cyclin D1( cyclin D1) protein levels were obvious reduced in propofol group( P<0.05 or P<0.01),the apoptosis rate,Bcl-2 related X protein( Bax) and cleaved cleaved caspase-3 protein levels were significantly increased( P<0.01). The Wnt/β-catenin activator LiCl attenuated the effect of propofol on the proliferation inhibition of SGC-7901 cells,and partially reversed the effect of propofol on the apoptosis induction of SGC-7901 cells. Conclusion: Propofol inhibits the proliferation of human gastric cancer SGC-7901 cells and promotes the apoptosis. The potential molecular mechanism is achieved by inhibiting Wnt/β-catenin signal transduction pathway.
作者
李加鹏
付倩琼
黄宏伟
Li Jiapeng;Fu Qianqiong;Huang Hongwei(Department of Anesthesiology,Central Hospital of Zaozhuang Mining Group,Shandong Zaozhuang 277000,China;Zaozhuang Mining Group Eastern Suburb Hospital)
出处
《中国药师》
CAS
2021年第1期59-63,共5页
China Pharmacist
