锌和N-乙酰半胱氨酸对镉致人正常肝细胞HL-7702凋亡的拮抗作用研究

目的：探讨氯化锌（ZnCl：）和N-乙酰半胱氨酸（N—acetylcysteine，NAC）对镉所致人正常肝细胞HL-7702凋亡的拮抗作用。方法：体外培养的人正常肝细胞HL-7702分别以0、10、20、40、80、160Ixmol／L的氯化镉（CdCl2）处理24h，ZnCl，和NAC顸处理组分别在各浓度的CdCl2处理前以25．0、50．0、100．0、200．0μmol／L的氯化锌和2．5、5．0、10．0、20．0mmol／LNAC预处理24h，MTT法测定各组HL-7702细胞的相对存活率；流式细胞术Annexin—V—PI双染法检测细胞凋亡百分率。结果：随着镉处理浓度的增加，氯化镉对细胞活力的抑制作用增强，40、80、160ixmol／L的镉处理组细胞相对存活率明显降低，50ixmol／L锌预处理组在CdCl：剂量为40、80μmol／L时，细胞相对存活率显著高于相应剂量的单纯镉处理组（P〈0．01），10mmol／LNAC预处理组只在40mmol／LCdCl2组细胞相对存活率显著高于相应剂量的单纯镉处理组（P〈0．05）；与0μmol／L镉处理组比较，40、80、160μmol／L镉处理组HL-7702细胞的凋亡百分率显著升高（P〈0．01）；与40μmol／L镉处理组比较，100μmol／L锌预处理组细胞凋亡率显著降低（P〈0．01）；5．0、10．0、20．0mmol／LNAC预处理可有效拮抗镉诱导的HL-7702细胞凋亡（P〈0．05）。结论：锌和NAC对镉致HL-7702细胞损伤和凋亡有明显的拮抗作用。

The Antagonism of Zinc and N-acetyl Cysteine on Apoptosis of HL-7702 Cells Induced by Cadmium

Objective： To study the antagonism of zinc chloride （ ZnCl2 ） and N-acetyl Cysteine （NAC） on apoptosis of normal human hepatoeyte HL-7702 cells induced by cadmium. Methods： Normal human hepatocyte HL-7702 ceils were incubated with 0, 10, 20, 40, 80, 160 μmol/L Cdcl2 for 24 h. The cells in groups of ZnC12 and NAC pretreatment were treated with 25.0, 50. 0, 100.0, 200.0 μmol/L ZnCl2 and2.5, 5.0, 10.0, 20.0 mmol/L NAC for24 h before incubated with 0, 10, 20, 40, 80, 160 μmol/L CdC12. Cells viability were measured by MTT. The rate of apoptosis was measured by Flowcytometry Staining of cells with phosphatidylserine （PS） -annexin- V. Results： The cells viability decreased obviously in the incubating cell with 40, 80, 160 μmol/L cadmium. The cells viability of 50. 0 μmol/L ZnC12 pretreatment group obviously increased compared with simple 40, 80 μmol/L cadmium incubating cell （P 〈 0. 01 ）. The cells viability of 10 mmol/L NAC pretreatment group increased compared with simple 40 μmol/L cadmium incubating cell （ P 〈 0. 05 ）. The apoptosis rate increased obviously in cells incubated with 40, 80, 160μmol/L cadmium compared with that in 0 p,mol/L cadmium group. The apoptosis rate in 100 μmol/L ZnC12 pretreatment decreased obriously compared with that in 40μmol/L codmium group and 5.0, 10. 0, 20. 0 mmol/L NAC pretreatment could suppress signifi- cantly cadmium-induced cell apoptosis （ P 〈 0. 05 ）. Conclusions ： ZnCl2 and NAC may suppress the apoptosis rate induced by cad- mium.