We have located links that may give you full text access.
Clofibrate Attenuates ROS Production by Lipid Overload in Cultured Rat Hepatoma Cells.
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.
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.
Full text links
Related Resources
Trending Papers
Challenges in Septic Shock: From New Hemodynamics to Blood Purification Therapies.Journal of Personalized Medicine 2024 Februrary 4
Molecular Targets of Novel Therapeutics for Diabetic Kidney Disease: A New Era of Nephroprotection.International Journal of Molecular Sciences 2024 April 4
The 'Ten Commandments' for the 2023 European Society of Cardiology guidelines for the management of endocarditis.European Heart Journal 2024 April 18
A Guide to the Use of Vasopressors and Inotropes for Patients in Shock.Journal of Intensive Care Medicine 2024 April 14
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app