eugenosedin-a and Disease-Models--Animal

eugenosedin-a has been researched along with Disease-Models--Animal* in 1 studies

Other Studies

1 other study(ies) available for eugenosedin-a and Disease-Models--Animal

Article	Year
Eugenosedin-A prevents high-fat diet increased adhesion molecules through inhibition of MAPK- and p65-mediated NF-κB pathway in rat model. The Journal of pharmacy and pharmacology, 2013, Volume: 65, Issue:2 Previous studies have shown eugenosedin-A, a 5-HT(1B/2A) and α(1)/α(2)/β(1)-adrenergic blocker, is able to decrease cholesterol levels, hyperglycaemia and inflammation in hyperlipidaemic mice induced by high-fat diet (HFD). The aim of this study is to examine the effects of eugenosedin-A on the inhibition of adhesion molecules of platelets, the aorta and acyl-coenzymeA:cholesterol acyltransferase-1 (ACAT-1) of macrophages in a hyperlipidaemic rat model.. Six-week-old Sprague-Dawley rats were randomly divided into two control and treatment groups. The control rats received either a regular diet or HFD and the treatment groups were fed HFD with either 5 mg/kg eugenosedin-A or atorvastatin for a 10-week period.. Compared with the two control groups, the HFD group had lower levels of high-density lipoprotein, higher concentrations of triglycerides, total cholesterol, low-density lipoprotein and insulin. The expression of adhesion molecules in platelets, aorta and monocyte-macrophage were enhanced by HFD. HFD also increased upstream proteins and their phosphorylated form in the aorta. In treatment groups, eugenosedin-A and atorvastatin improved HFD-induced hyperlipidaemia and levels of insulin. Eugenosedin-A reduced the upregulation of P-selectin, ICAM-1, ICAM-2, ICAM-3, VCAM, PECAM in platelets and inhibited E-selectin, ICAM-1, ICAM-2, ICAM-3, VCAM and PECAM protein levels in the aorta. Eugenosedin-A reduced the ACAT-1 protein expression of monocyte-macrophages. The expression of PKCα, MAPKs, IKKα and p65 and their phosphorylated form were reduced in treatment groups.. Taken together, hyperlipidaemia enhances the expression of adhesion molecules and ACAT-1 protein, and eugenosedin-A ameliorates those increases. Through inhibition of MAPK- and p-65-mediated NF-κB pathway, eugenosedin-A decreases the quantity of adhesion molecules. Topics: Acetyl-CoA C-Acetyltransferase; Animals; Aorta; Blood Platelets; Body Weight; Cell Adhesion Molecules; Diet, High-Fat; Disease Models, Animal; E-Selectin; Hyperlipidemias; Macrophages; Male; Mitogen-Activated Protein Kinase Kinases; NF-kappa B; Piperazines; Random Allocation; Rats; Rats, Sprague-Dawley; Signal Transduction; Transcription Factor RelA	2013

Article

Year

Eugenosedin-A prevents high-fat diet increased adhesion molecules through inhibition of MAPK- and p65-mediated NF-κB pathway in rat model.

The Journal of pharmacy and pharmacology, 2013, Volume: 65, Issue:2

Previous studies have shown eugenosedin-A, a 5-HT(1B/2A) and α(1)/α(2)/β(1)-adrenergic blocker, is able to decrease cholesterol levels, hyperglycaemia and inflammation in hyperlipidaemic mice induced by high-fat diet (HFD). The aim of this study is to examine the effects of eugenosedin-A on the inhibition of adhesion molecules of platelets, the aorta and acyl-coenzymeA:cholesterol acyltransferase-1 (ACAT-1) of macrophages in a hyperlipidaemic rat model.. Six-week-old Sprague-Dawley rats were randomly divided into two control and treatment groups. The control rats received either a regular diet or HFD and the treatment groups were fed HFD with either 5 mg/kg eugenosedin-A or atorvastatin for a 10-week period.. Compared with the two control groups, the HFD group had lower levels of high-density lipoprotein, higher concentrations of triglycerides, total cholesterol, low-density lipoprotein and insulin. The expression of adhesion molecules in platelets, aorta and monocyte-macrophage were enhanced by HFD. HFD also increased upstream proteins and their phosphorylated form in the aorta. In treatment groups, eugenosedin-A and atorvastatin improved HFD-induced hyperlipidaemia and levels of insulin. Eugenosedin-A reduced the upregulation of P-selectin, ICAM-1, ICAM-2, ICAM-3, VCAM, PECAM in platelets and inhibited E-selectin, ICAM-1, ICAM-2, ICAM-3, VCAM and PECAM protein levels in the aorta. Eugenosedin-A reduced the ACAT-1 protein expression of monocyte-macrophages. The expression of PKCα, MAPKs, IKKα and p65 and their phosphorylated form were reduced in treatment groups.. Taken together, hyperlipidaemia enhances the expression of adhesion molecules and ACAT-1 protein, and eugenosedin-A ameliorates those increases. Through inhibition of MAPK- and p-65-mediated NF-κB pathway, eugenosedin-A decreases the quantity of adhesion molecules.

Topics: Acetyl-CoA C-Acetyltransferase; Animals; Aorta; Blood Platelets; Body Weight; Cell Adhesion Molecules; Diet, High-Fat; Disease Models, Animal; E-Selectin; Hyperlipidemias; Macrophages; Male; Mitogen-Activated Protein Kinase Kinases; NF-kappa B; Piperazines; Random Allocation; Rats; Rats, Sprague-Dawley; Signal Transduction; Transcription Factor RelA

2013