BAPTA-AM指质体通过恢复胞质钙稳态抑制D-GalN致HepG-2细胞凋亡

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AnnexinⅤ-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。

BAPTA-AM Liposome Protects HepG-2 Cells from D-GalN-induced Apoptosis Via Calcium Homeostasis Resumption

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＋]iwas 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 homeostasis and maintain cell morphology,but the protective effect of BAPTA-AM liposome could be antagonized by A23187.Ca2＋]iwas negatively correlated with cell viability to some extent. Conclusion BAPTA-AM shows an inhibitory effect on D-GalN-induced HepG-2 cell injury by alleviating the calcium overload.