l-663536 and Hypercholesterolemia

l-663536 has been researched along with Hypercholesterolemia* in 1 studies

Other Studies

1 other study(ies) available for l-663536 and Hypercholesterolemia

Article	Year
Identification of Picrasidine C as a Subtype-Selective PPARα Agonist. Journal of natural products, 2016, Dec-23, Volume: 79, Issue:12 Picrasidine C (1), a dimeric β-carboline-type alkaloid isolated from the root of Picrasma quassioides, was identified to have PPARα agonistic activity by a mammalian one-hybrid assay from a compound library. Among the PPAR subtypes, 1 selectively activated PPARα in a concentration-dependent manner. Remarkably, 1 also promoted PPARα transcriptional activity by a peroxisome proliferator response element-driven luciferase reporter assay. Furthermore, 1 induced the expression of PPARα-regulated genes involved in lipid, glucose, and cholesterol metabolism, such as CPT-1, PPARα, PDK4, and ABCA1, which was abrogated by the PPARα antagonist MK-886, indicating that the effect of 1 was dependent on PPARα activation. This is the first report to demonstrate 1 to be a subtype-selective PPARα agonist with potential application in treating metabolic diseases, such as hyperlipidemia, atherosclerosis, and hypercholesterolemia. Topics: Alkaloids; Animals; Atherosclerosis; Carbolines; Cholesterol; Glucose; Hypercholesterolemia; Indoles; Lipid Metabolism; Lipids; Mice; Molecular Structure; Picrasma; PPAR alpha; Transcription Factors	2016

Article

Year

Identification of Picrasidine C as a Subtype-Selective PPARα Agonist.

Journal of natural products, 2016, Dec-23, Volume: 79, Issue:12

Picrasidine C (1), a dimeric β-carboline-type alkaloid isolated from the root of Picrasma quassioides, was identified to have PPARα agonistic activity by a mammalian one-hybrid assay from a compound library. Among the PPAR subtypes, 1 selectively activated PPARα in a concentration-dependent manner. Remarkably, 1 also promoted PPARα transcriptional activity by a peroxisome proliferator response element-driven luciferase reporter assay. Furthermore, 1 induced the expression of PPARα-regulated genes involved in lipid, glucose, and cholesterol metabolism, such as CPT-1, PPARα, PDK4, and ABCA1, which was abrogated by the PPARα antagonist MK-886, indicating that the effect of 1 was dependent on PPARα activation. This is the first report to demonstrate 1 to be a subtype-selective PPARα agonist with potential application in treating metabolic diseases, such as hyperlipidemia, atherosclerosis, and hypercholesterolemia.

Topics: Alkaloids; Animals; Atherosclerosis; Carbolines; Cholesterol; Glucose; Hypercholesterolemia; Indoles; Lipid Metabolism; Lipids; Mice; Molecular Structure; Picrasma; PPAR alpha; Transcription Factors

2016