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

Authors
 Geun Hye Hwang  ;  Yu Jin Jeon  ;  Ho Jae Han  ;  Soo Hyun Park  ;  Kyoung Min Baek  ;  Woochul Chang  ;  Joong Sun Kim  ;  Lark Kyun Kim  ;  You-Mie Lee  ;  Sangkyu Lee  ;  Jong-Sup Bae  ;  Jun-Goo Jee  ;  Min Young Lee 
Citation
 JOURNAL OF VETERINARY SCIENCE, Vol.16(1) : 17-23, 2015 
Journal Title
JOURNAL OF VETERINARY SCIENCE
ISSN
 1229-845X 
Issue Date
2015
MeSH
Animals ; Apoptosis/drug effects* ; Butylated Hydroxyanisole/chemistry ; Butylated Hydroxyanisole/pharmacology* ; Cell Survival/drug effects ; Cells, Cultured ; Hepatocytes/drug effects* ; Hydrogen Peroxide/toxicity* ; Male ; Mice ; Mice, Inbred ICR ; Molecular Structure
Keywords
apoptosis ; butylated hydroxyanisole ; primary mouse hepatocytes ; reactive oxygen species
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.
Files in This Item:
T201506197.pdf Download
DOI
10.4142/jvs.2015.16.1.17
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Kim, Lark Kyun(김락균) ORCID logo https://orcid.org/0000-0001-5983-4470
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/157310
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