邻苯二甲酸二（2-乙基己基）酯诱导 HepG2 细胞线粒体膜电位丧失和 Caspase3 激活。
Mono-2-ethylhexyl phthalate induced loss of mitochondrial membrane potential and activation of Caspase3 in HepG2 cells.
机构信息
Department of Occupational and Environmental Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China.
出版信息
Environ Toxicol Pharmacol. 2012 May;33(3):421-30. doi: 10.1016/j.etap.2012.02.001. Epub 2012 Feb 10.
L02 and HepG2 cells were exposed to mono-(2-ethylhexyl) phthalate (MEHP) at concentrations of 6.25-100μM. After 48h treatment, MEHP decreased HepG2 cell viability in a concentration-dependent manner and L02 cell viability in the 50 and 100μM groups (p<0.01). Furthermore, at 24 and 48h after treatment, MEHP decreased the glutathione levels of HepG2 cells in all treatment groups and in the ΔΨ(m) in L02 and HepG2 cells with MEHP≥25μM (p<0.05 or p<0.01). At 24h after treatment, MEHP induced activation of caspase3 in all treated HepG2 and L02 cells (p<0.05 or p<0.01) except the 100μM MEHP treatment group. The increase in the Bax to Bcl-2 ratio suggests that Bcl-2 family involved in the control of MEHP-induced apoptosis in these two cell types. The data suggest that MEHP could induce apoptosis of HepG2 cells through mitochondria- and caspase3-dependent pathways.
L02 和 HepG2 细胞分别暴露于浓度为 6.25-100μM 的单-(2-乙基己基)邻苯二甲酸酯 (MEHP) 中。经过 48 小时处理后，MEHP 呈浓度依赖性降低 HepG2 细胞活力，且在 50 和 100μM 组中 L02 细胞活力降低（p<0.01）。此外，在处理后 24 和 48 小时，MEHP 降低了所有处理组 HepG2 细胞中的谷胱甘肽水平，以及 MEHP≥25μM 时 L02 和 HepG2 细胞中的 ΔΨ(m)（p<0.05 或 p<0.01）。在处理后 24 小时，除 100μM MEHP 处理组外，MEHP 诱导所有处理的 HepG2 和 L02 细胞中 caspase3 的激活（p<0.05 或 p<0.01）。Bax 与 Bcl-2 比值的增加表明 Bcl-2 家族参与了这两种细胞类型中 MEHP 诱导的细胞凋亡的调控。数据表明，MEHP 可能通过线粒体和 caspase3 依赖性途径诱导 HepG2 细胞凋亡。
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