Hyperlipidemia is a known cause of coronary
vascular diseases, which is a major cause of death in many parts of the world. Targeting several pathways that lead to increase in
lipid profiles is of great potential to control diseases. 1H-indole-2-carboxamide derivatives were tested for their hypolipidemic activity at the molecular level in comparison with
bezafibrate. The gene expression profiles of
lipoprotein signaling and
cholesterol metabolism and
fatty acid metabolism PCR arrays were determined in rats with acute
hyperlipidemia induced by Triton WR1339.
Lipid profiles of serum from treated rats showed significant hypolipidemic effect by the compounds. Several genes of potential interest were reported to be overexpressed by Triton WR1339 including Apoc3,
Apob, Hmgcs2, Apoa1,
Apoe, Apof, acsl1, and Decr1. Most of the overexpressed genes were downregulated by N-(3-Benzoylphenyl)-1H-Indole-2-Carboxamide with significant decreases in Apoc3,
Apob, Acaa2, Acsl1, and Slc247a5 gene expression levels. N-(4-Benzoylphenyl)-1H-Indole-2-Carboxamide and
bezafibrate did not significantly affect the gene expression levels which were increased with acute
hyperlipidemia induced by Triton WR1339. In conclusion, gene expression profiling identified the possible mechanism in which Triton WR1339 induces its acute hyperlipidemic effect which was reversed by the use of N-(3-Benzoylphenyl)-1H-Indole-2-Carboxamide.