Clofibrate Attenuates ROS Production by Lipid Overload in Cultured Rat Hepatoma Cells.

Abstract:

PURPOSE:To investigate the effect of clofibrate on inducing liver fatty acid binding protein (FABP1) following a high-fat load in a hepatocyte cell culture model. METHODS:Rat hepatoma cells (CRL-1548) were treated with a fatty acid (FA) mixture consisting of oleate:palmitate (2:1) in the presence of 3% albumin. Cells were treated with 0, 0.5, 1, 2, or 3 mM FA for 24 and 48 hr, or further treated with 500 µM clofibrate (CLO) to induce FABP1 levels. Cytotoxicity was determined using the WST-1 assay. Intracellular lipid droplets were quantitated following staining with Nile Red. Dichlorofluorescein (DCF) was used to assess the extent of intracellular reactive oxygen species (ROS). RESULTS:Cell viability decreased (p < 0.01) with an increase in lipid concentration. Intracellular lipid droplets accumulated significantly (p < 0.001) with an increase in long-chain fatty acid load, which was associated with a statistical increase (p < 0.05) in ROS levels. Early clofibrate treatment showed significant increases in intracellular FABP1 levels with significant decreases in ROS levels (p < 0.05). Silencing FABP1 expression using siRNA revealed that FABP1 was the main contributor for the observed intracellular ROS clearance. CONCLUSIONS:Characteristic cellular damage resulted from released ROS following a high fat load to hepatoma cells. The damage was attenuated through early treatment with clofibrate, which may act as a hepatoprotectant by inducing FABP1 expression and in this manner, suppress intracellular ROS levels. This article is open to POST-PUBLICATION REVIEW. Registered readers (see "For Readers") may comment by clicking on ABSTRACT on the issue's contents page.

journal_name

J Pharm Pharm Sci

authors

Chen Y,Li W,Wang G,Burczynski FJ

doi

10.18433/J3TS70

subject

Has Abstract

pub_date

2017-01-01 00:00:00

pages

239-251

issn

1482-1826

journal_volume

20

pub_type

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