Effect of CLA (Conjugated Linoleic Acid) on the Anti-Atherosclerotic Factors in Human Hepatoma HepG2 Cells.
- Author:
Hyunhee OH
1
;
Hejung MUN
;
Myoungsook LEE
Author Information
1. Department of Food and Nutrition, Sungshin Women's University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
conjugated linoleic acid (CLA);
HepG2 cell;
lipid peroxidation;
prostagladin E2 (PGE2);
thromboxane A2 (TXA2)
- MeSH:
Anticarcinogenic Agents;
Arachidonic Acid;
Arachidonic Acids;
Atherosclerosis;
Carcinoma, Hepatocellular*;
Cell Death;
Cell Membrane;
Cell Proliferation;
Dairy Products;
Dinoprostone;
Eicosanoids;
Fatty Acids;
Hep G2 Cells*;
Humans*;
Linoleic Acid;
Lipid Peroxidation;
Lipid Peroxides;
Liver;
Meat;
Membranes;
Metabolism;
Thromboxane A2
- From:The Korean Journal of Nutrition
2004;37(3):182-192
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Conjugated linoleic acid (CLA) is the mixture of positional and geometric isomers of linoleic acid (LA), which is found abundantly in dairy products and meats. This study was performed to investigate the anticarcinogenic effect of CLA in HepG2 hepatoma cells. HepG2 cell were treated with LA and CLA at the various concentrations of 10, 20, 40, 80 uM each at different incubation times. After each incubation times, cell proliferation, fatty acids incorporation into cell, peroxidation and postaglandin E2 (PGE2) and thromboxane A2 (TXA2) for the eicosanoid metabolism were measured. LA treated HepG2 cells were increased cell growth 6 - 70% of control whereas CLA increased cell death the half of those in LA group (p < 0.001). LA and CLA were incorporated very well into the cellular membranes four times higher than in control according to concentration and longer incubation times. Moreover, LA synthesized significantly arachidonic acids corresponding with LA concentration compared to CLA supplementation. The supplementation with LA increased intracellular lipid peroxides concentration corresponding with LA concentration and five times higher than those in CLA significantly at any incubation times (p < 0.001). PGE2 and TXA2 levels were three to twenty times lower in condition of CLA treatments than LA, respectively. Overall, the dietary CLA might change the HepG2 cell growth by the changes of cell composition, production of lipid peroxide. Since CLA have not changed the levels of arachidonic acid of cell membrane, which was sources of eicosanoids, eicosanoid synthesis was not increased in CLA compared to LA. Our results was suggest CLA has a possibility to protect the progress of atherosclerosis because CLA does not produce lipid production and endothelial contraction factors in liver.
