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丁基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。

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

作者信息

Hwang Geun Hye, Jeon Yu Jin, Han Ho Jae, Park Soo Hyun, Baek Kyoung Min, Chang Woochul, Kim Joong Sun, Kim Lark Kyun, Lee You-Mie, Lee Sangkyu, Bae Jong-Sup, Jee Jun-Goo, Lee Min Young

机构信息

College of Pharmacy, Research Institute of Pharmaceutical Sciences, Kyungpook National University, Daegu 702-701, Korea.

Department of Veterinary Physiology, College of Veterinary Medicine, Seoul National University, Seoul 151-742, Korea.

出版信息

J Vet Sci. 2015;16(1):17-23. doi: 10.4142/jvs.2015.16.1.17. Epub 2015 Mar 18.

Abstract

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.

摘要

丁基羟基茴香醚(BHA)是一种合成酚类化合物,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。我们研究了BHA对原代培养的小鼠肝细胞中过氧化氢(H2O2)诱导的细胞凋亡的影响。H2O2以剂量依赖性方式显著降低细胞活力。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预处理可显著减轻H2O2诱导的细胞活力下降。H2O2暴露导致细胞内活性氧(ROS)生成增加,而用BHA或N-乙酰半胱氨酸(NAC,一种ROS清除剂)预处理可显著抑制这种增加。用BHA和NAC预处理也可减轻H2O2诱导的细胞活力下降。此外,BHA还抑制H2O2诱导的Bax增加、Bcl-2降低和PARP-1裂解。综上所述,本研究结果表明,BHA通过抑制ROS生成来保护原代培养的小鼠肝细胞免受H2O2诱导的细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/013d/4367145/c503821927f8/jvs-16-17-g001.jpg

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