探讨二氯化钴（CoCl₂）所致缺氧对HepG2细胞增殖抑制和凋亡的影响以及可能机制。

采用CoCl₂模拟低氧环境处理细胞，Western Blotting法测定胞质蛋白Caspase-3蛋白的表达；噻唑蓝（MTT）法检测细胞的增殖情况；AnnexinV-FITC/PI双标记染色，流式细胞术检测不同CoCl₂浓度作用使缺氧肿瘤细胞的凋亡情况。

低氧处理后胞质Caspase-3的活性增加，表达呈现浓度依赖性；细胞增殖抑制作用表现出浓度依赖性抑制作用；流式细胞仪检测结果显示，正常对照组以及50、100、200、300、500 μmol/L CoCl₂模拟低氧组的细胞生长抑制率分别为（0.42±0.21）%、（1.22±0.41）%、（7.61±0.66）%、（13.31±0.97）%、（20.41±0.78）%和（28.56±0.96）%。

Caspase-3在肝癌发生发展过程中扮演重要的角色，在低氧情况下对HepG2细胞生长和分化具有调控作用。CoCl₂可能通过上调Caspase-3的表达，从而对肝癌细胞发挥抑制细胞增殖和诱导凋亡的作用。

To investigate the proliferation and apoptosis of HepG2 cell under hypoxia induced by cobalt-chloride.

HepG2 cells were deal with CoCl₂ which was adopted to simulate low oxygen environment. The expression level of cytoplasmic protein Caspase 3 was measured by Western Blotting. The cell proliferation was detected by MTT assay. AnnexinV-FITC/PI double labeling staining and flow cytometry were used to test tumor cell apoptosis under oxygen deficiency with different CoCl₂ concentration.

The cytoplasmic Caspase 3 activity increased after low oxygen treatment, and expression suggested concentration-dependency, the same with the inhibition on the proliferative capabilities of HepG2 cells. Flow cytometry showed that the cell apoptosis rates of control group, the hypoxic groups of 50, 100, 200, 300, 500 μmol/L CoCl₂ were (0.42 ± 0.21)%, (1.22 ± 0.41)%, (7.61 ± 0.66)%, (13.31 ± 0.97)%, (20.41 ± 0.78)% and (28.56 ± 0.96)%.

Caspase-3 may play an important role in the development of liver cancers. Under hypoxic condition, it can regulate cell growth and differentiation. CoCl₂ inhibits the HepG2 cells proliferation and stimulates their apoptosis by up-regulating Caspase-3.