论文部分内容阅读
目的探讨亚砷酸钠对人正常肝(L-02)细胞凋亡及Bax、Bcl-2 m RNA和蛋白表达的影响。方法将L-02肝细胞分别暴露于含0(对照)、50、100、150μmol/L亚砷酸钠的培养基中暴露24 h。采用MTT法检测L-02肝细胞的存活率,采用流式细胞术检测L-02肝细胞凋亡率,采用RT-PCR的方法检测Bax、Bcl-2 m RNA相对表达情况,采用Westernblotting方法检测L-02肝细胞中Bax、Bcl-2蛋白的表达情况。结果与对照组相比,各浓度亚砷酸钠染毒组L-02细胞的存活率均较低,凋亡率均较高,差异均有统计学意义(P<0.05);且随着亚砷酸钠染毒浓度的升高,L-02细胞的存活率呈下降趋势,而凋亡率上升趋势。与对照组相比,各浓度亚砷酸钠染毒组L-02细胞中Bcl-2、Bax m RNA和蛋白的表达水平均较高,100μmol/L亚砷酸钠染毒组Bcl-2 m RNA/Bax m RNA值也较高,而150μmol/L亚砷酸钠染毒组Bcl-2 m RNA/Bax m RNA值及50、150μmol/L亚砷酸钠染毒组Bcl-2蛋白/Bax蛋白值均较低,差异均有统计学意义(P<0.05)。结论亚砷酸钠可抑制L-02肝细胞的生长,诱导细胞凋亡的发生;其机制可能与Bcl-2家族的激活有关。
Objective To investigate the effects of sodium arsenite on the apoptosis of human normal liver (L-02) cells and the expression of Bax, Bcl-2 mRNA and m RNA. Methods L-02 hepatocytes were exposed to culture medium containing 0 (control), 50, 100, 150 μmol / L sodium arsenite for 24 h. The survival rate of L-02 hepatocytes was detected by MTT method. The apoptosis rate of L-02 hepatocytes was detected by flow cytometry. The relative expression of Bax and Bcl-2 mRNA was detected by RT-PCR and Western blotting Expression of Bax and Bcl-2 in L-02 hepatocytes. Results Compared with the control group, the survival rates of L-02 cells were lower and the apoptosis rates were higher in the arsenite-treated groups (P <0.05) Sodium arsenate exposure concentration, L-02 cell survival rate decreased, while the apoptotic rate increased. Compared with the control group, the expression levels of Bcl-2, Bax m RNA and protein in L-02 cells treated with sodium arsenite at various concentrations were higher than those in the control group, while the Bcl-2 m Bcl-2 mRNA / Bax m RNA in 150μmol / L sodium arsenite treatment group and Bcl-2 protein / Bax in 50,150μmol / L sodium arsenite treatment group were higher than those in control group Protein values were lower, the differences were statistically significant (P <0.05). Conclusion Sodium arsenite inhibits the growth of L-02 hepatocytes and induces apoptosis. The mechanism may be related to the activation of Bcl-2 family.