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目的：探讨1，2-二（2-氨基苯氧基）乙烷-N，N，N'，N'-四乙酸四乙酰氧甲基酯（ BAPTA-AM）恢复胞质钙离子稳态后对D-GalN诱导HepG-2细胞凋亡的影响。方法建立D-GalN诱导HepG-2细胞凋亡模型，采用MTT比色法、台盼蓝染色及Annexin Ⅴ-EGFP、Hoechst-33258荧光染色等考察HepG-2细胞活性及细胞凋亡情况；通过Fura-2/AM钙离子荧光探针法测定不同处理组细胞内游离钙浓度，初步评价钙离子稳态与细胞凋亡的关系。结果 BAPTA-AM脂质体能显著抑制D-GalN致胞质钙离子浓度的升高，恢复胞质钙稳态，维持细胞形态，减少D-GalN诱导细胞凋亡。在一定范围内，细胞内钙离子浓度的增加与细胞活性的提高呈负相关，且钙离子载体 A23187能够拮抗BAPTA-AM脂质体对HepG-2细胞的保护作用。结论BAPTA-AM脂质体通过减轻钙超载，抑制D-GalN诱导HepG-2细胞凋亡。“,”Objective To investigate the effect of calcium homeostasis post BAPTA-AM liposome treatment on D-GalN-induced HepG-2 cell apoptosis. Methods The viability of HepG-2 cells was evaluated via MTT assay and tryban blue staining. Hoechst-33258 and Annexin V-EGFP were used to indicate the apoptosis.[ Ca2+]i was tested via the calcium fluorescence probe Fura-2/AM and the relationship between calcium homeostasis and apoptosis was studied. Results BAPTA-AM could significantly alleviate the accumulation of cytosolic calcium,resume calcium ho-meostasis and maintain cell morphology,but the protective effect of BAPTA-AM liposome could be antagonized by A23187.[Ca2+]i was negatively correlated with cell viability to some extent. Conclusion BAPTA-AM shows an in-hibitory effect on D-GalN-induced HepG-2 cell injury by alleviating the calcium overload.