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Protective effect of butylated hydroxylanisole against hydrogen peroxide-induced apoptosis in primary cultured mouse hepatocytes

机译:丁基化羟基茴香醚对过氧化氢诱导的原代培养小鼠肝细胞凋亡的保护作用

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摘要

Butylated hydroxyanisole (BHA) is a synthetic phenolic compound consisting of a mixture of two isomeric organic compounds: 2-tert-butyl-4-hydroxyanisole and 3-tert-butyl-4-hydroxyanisole. We examined the effect of BHA against hydrogen peroxide (H2O2)-induced apoptosis in primary cultured mouse hepatocytes. Cell viability was significantly decreased by H2O2 in a dose-dependent manner. Additionally, H2O2 treatment increased Bax, decreased Bcl-2, and promoted PARP-1 cleavage in a dose-dependent manner. Pretreatment with BHA before exposure to H2O2 significantly attenuated the H2O2-induced decrease of cell viability. H2O2 exposure resulted in an increase of intracellular reactive oxygen species (ROS) generation that was significantly inhibited by pretreatment with BHA or N-acetyl-cysteine (NAC, an ROS scavenger). H2O2-induced decrease of cell viability was also attenuated by pretreatment with BHA and NAC. Furthermore, H2O2-induced increase of Bax, decrease of Bcl-2, and PARP-1 cleavage was also inhibited by BHA. Taken together, results of this investigation demonstrated that BHA protects primary cultured mouse hepatocytes against H2O2-induced apoptosis by inhibiting ROS generation.
机译:丁基羟基茴香醚(BHA)是一种合成的酚类化合物,由两种异构有机化合物的混合物组成:2-叔丁基-4-羟基茴香醚和3-叔丁基-4-羟基茴香醚。我们检查了BHA对过氧化氢(H2O2)诱导的原代培养小鼠肝细胞凋亡的影响。 H2O2以剂量依赖的方式显着降低了细胞活力。此外,H2O2处理以剂量依赖性方式增加Bax,降低Bcl-2并促进PARP-1裂解。在暴露于H2O2之前用BHA进行预处理可以显着减弱H2O2诱导的细胞活力下降。暴露于H2O2导致细胞内活性氧(ROS)生成增加,而BHA或N-乙酰基半胱氨酸(NAC,ROS清除剂)预处理可显着抑制细胞内活性氧的生成。用BHA和NAC预处理还可以减轻H2O2诱导的细胞活力的降低。此外,BHA还抑制了H2O2诱导的Bax升高,Bcl-2降低和PARP-1裂解。两者合计,这项研究的结果表明BHA通过抑制ROS的生成来保护原代培养的小鼠肝细胞免受H 2 O 2 诱导的凋亡。

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