Inhibitory effects of tilianin on the expression of inducible nitric oxide synthase in low density lipoprotein receptor deficiency mice.
- Author:
Ki Hoan NAM
;
Jae Hoon CHOI
;
Yun Jeong SEO
;
Young Mi LEE
;
Yong Sung WON
;
Mi Ran LEE
;
Mi Ni LEE
;
Jong Gil PARK
;
Young Myeong KIM
;
Hyoung Chin KIM
;
Chul Ho LEE
;
Hyeong Kyu LEE
;
Sei Ryang OH
;
Goo Taeg OH
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
anti-inflammatory agents;
hyperlipoproteinemia;
nitric oxide synthase type II;
nitric oxide;
tilianin
- MeSH:
Tyrosine/analogs & derivatives/metabolism;
Tissue Distribution;
Sinus of Valsalva/metabolism/pathology/ultrastructure;
Receptors, LDL/*genetics;
Promoter Regions (Genetics)/drug effects;
Nitric Oxide Synthase Type II/*metabolism;
Nitric Oxide/biosynthesis/blood;
NF-kappa B/metabolism;
Mice, Knockout;
Mice;
Male;
Inflammation/metabolism;
Glycosides/*pharmacology;
Flavonoids/*pharmacology;
Down-Regulation/drug effects;
Atherosclerosis/metabolism;
Animals
- From:Experimental & Molecular Medicine
2006;38(4):445-452
- CountryRepublic of Korea
- Language:English
-
Abstract:
We investigated the effect of tilianin upon inducible nitric oxide synthesis in the plasma of low-density lipoprotein receptor knock-out (Ldlr-/-) mice fed with high cholesterol diet and in primary peritoneal macrophages of Ldlr-/- mice. High cholesterol diet induced nitric oxide production in the plasma of Ldlr-/- mice. Tilianin reduced the level of nitric oxide (NO) in plasma from Ldlr-/- mice induced by the high cholesterol diet. Tilianin also inhibited the NO production from the primary culture of peritoneal macrophages treated with lipopolysaccharide. The inhibition of NO production was caused by the suppression of inducible nitric oxide synthase (iNOS) gene expression in peritoneal macrophages isolated from Ldlr-/- mice. Moreover, tilianin inhibited the transcriptional activation of iNOS promoter that has NF-kappa B binding element. Thus, these results provide the first evidence that tilianin inhibit iNOS expression and production of NO and may act as a potential anti-inflammatory agent.
