Hepatoprotective role of liver fatty acid binding protein in acetaminophen induced toxicity

BMC Gastroenterology

Frank J Burczynski¹  Yufei Chen²  Jing Yan²  Yuewen Gong²  Guqi Wang³  Yu Gong² 

[1] Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Manitoba, Winnipeg, MB, Canada;Faculty of Pharmacy, University of Manitoba, 750 McDermot Avenue, Winnipeg, MB R3E 0T5, Canada;Liver-Biliary-Pancreatic Center, Carolinas Medical Center Charlotte, Charlotte, NC 28232-2861, USA

关键词: Apoptosis;    Liver;    Oxidative stress;    Acetaminophen;    FABP1;   

Others  :  855677
DOI  :  10.1186/1471-230X-14-44

 received in 2013-04-30, accepted in 2014-03-03,  发布年份 2014

【 摘 要 】

Background

FABP1 has been reported to possess strong antioxidant properties. Upon successful transfection of the Chang cell line, which has undetectable FABP1 mRNA levels, with human FABP1 cDNA, the Chang cells were shown to express FABP1. Using the transfected and control (normal) Chang cells and subjecting them to oxidative stress, transfected cells were reported to be associated with enhanced cell viability. This study extends those observations by investigating the effect of FABP1 on acetaminophen (AAP)-induced hepatotoxicity. We hypothesized that presence of FABP1 would enhance cell viability compared to control cells (vector transfected cells).

Methods

Following AAP treatment of Chang FABP1 transfected and control cells, cell viability, oxidative stress, and apoptosis were evaluated using lactate dehydrogenase (LDH) release, the fluorescent probe DCF, and Bax expression, respectively.

Results

FABP1 cDNA transfected cells showed greater resistance against AAP toxicity than vector transfected cells. Significantly lower LDH levels (p < 0.05) were observed as were lower DCF fluorescence intensity (p < 0.05) in FABP1 cDNA transfected cells compared to vector transfected cells. FABP1 expression also attenuated the expression of Bax following AAP induced toxicity.

Conclusion

FABP1 attenuated AAP-induced toxicity and may be considered a cytoprotective agent in this in vitro model of drug induced oxidative stress.

【 授权许可】

   
2014 Gong et al.; licensee BioMed Central Ltd.

【 图 表 】

【 参考文献 】

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