Javascript must be enabled to continue!
GW24-e2393 The effect of rosuvastatin on reendothelialisation of late endothelial outgrowth cell influenced by C-reactive protein
View through CrossRef
Objectives
To observe whether CRP influenced expressions of eNOS/NO in late endothelial outgrowth cells (EOCs) though signalling pathway mediated by receptor for advanced glycation end products (RAGE), and whether rosuvastatin could improve EOCs’ reendothelialisation influenced by CRP though restraining RAGE.
Methods
The EOCs were treated with CRP of different concentrations and treating times, and EOCs were pre-incubated with rosuvastatin of different concentrations and then stimulated with 50ug/ml CRP. The eNOS of EPCs were measured by quantitative PCR and NO secretions were detected by NO nitrate reductive enzymatic. The RAGE protein expressions were checked by western blotting. MTT assay was used to test proliferation of EPCs, transwell assay for migration, and adhesiveness assay for adhesion.
Results
The eNOS mRNA expression and NO secretions decreased significantly with CRP-stimulated concentration and time, and down-regulated by rosuvastatin. Also, the RAGE protein expression rised in a dose-dependent and time-dependent manner. The RAGE was significantly decreased by rosuvastatin with different dosages. After treatment with different dosage rosuvastatin, the vitro functions (migration and adhesion) of CRP-influenced EOCs were dosage-dependently upregulated. However, the proliferation had no changes.
Conclusions
CRP could influence expressions of eNOS/NO though signalling pathway mediated by RAGE. Rosuvastatin could improve EOCs’ reendothelialisation influenced by CRP though restraining RAGE.
Title: GW24-e2393 The effect of rosuvastatin on reendothelialisation of late endothelial outgrowth cell influenced by C-reactive protein
Description:
Objectives
To observe whether CRP influenced expressions of eNOS/NO in late endothelial outgrowth cells (EOCs) though signalling pathway mediated by receptor for advanced glycation end products (RAGE), and whether rosuvastatin could improve EOCs’ reendothelialisation influenced by CRP though restraining RAGE.
Methods
The EOCs were treated with CRP of different concentrations and treating times, and EOCs were pre-incubated with rosuvastatin of different concentrations and then stimulated with 50ug/ml CRP.
The eNOS of EPCs were measured by quantitative PCR and NO secretions were detected by NO nitrate reductive enzymatic.
The RAGE protein expressions were checked by western blotting.
MTT assay was used to test proliferation of EPCs, transwell assay for migration, and adhesiveness assay for adhesion.
Results
The eNOS mRNA expression and NO secretions decreased significantly with CRP-stimulated concentration and time, and down-regulated by rosuvastatin.
Also, the RAGE protein expression rised in a dose-dependent and time-dependent manner.
The RAGE was significantly decreased by rosuvastatin with different dosages.
After treatment with different dosage rosuvastatin, the vitro functions (migration and adhesion) of CRP-influenced EOCs were dosage-dependently upregulated.
However, the proliferation had no changes.
Conclusions
CRP could influence expressions of eNOS/NO though signalling pathway mediated by RAGE.
Rosuvastatin could improve EOCs’ reendothelialisation influenced by CRP though restraining RAGE.
Related Results
Rosuvastatin Alone or With Extended‐Release Niacin: A New Therapeutic Option for Patients With Combined Hyperlipidemia
Rosuvastatin Alone or With Extended‐Release Niacin: A New Therapeutic Option for Patients With Combined Hyperlipidemia
Combination therapy with a statin and niacin may provide optimal therapy for patients with combined hyperlipidemia and low levels of highdensity lipoprotein (HDL) cholesterol. The ...
GW24-e0760 Effects of rosuvastatin on rats with dyslipidemia and antiatherosclerotic
GW24-e0760 Effects of rosuvastatin on rats with dyslipidemia and antiatherosclerotic
Objectives
To explore the regulating lipid effects of Rosuvastatin on rats with dyslipidemia and its antiatherosclerotic effects.
...
Comparison Between Atorvastatin and Rosuvastatin on Anti- Thrombogenic Effect in Patients with Hyperlipidemia
Comparison Between Atorvastatin and Rosuvastatin on Anti- Thrombogenic Effect in Patients with Hyperlipidemia
Background: Atorvastatin and rosuvastatin are two widely used HMG-CoA reductase inhibitors (statins). These are used as lipid-lowering drugs to reduce atherosclerosis-induced cardi...
Endothelial Protein C Receptor
Endothelial Protein C Receptor
IntroductionThe protein C anticoagulant pathway plays a critical role in the negative regulation of the blood clotting response. The pathway is triggered by thrombin, which allows ...
Entanglement of AGE-RAGE axis in cardiac pathosis
Entanglement of AGE-RAGE axis in cardiac pathosis
AbstractCardiovascular diseases are the major cause of death globally. Acute coronary syndrome is one of numerous cardiovascular illnesses, including advanced glycation end product...
C-MET OVEREXPRESSION PROMOTE REENDOTHELIALISATION AND INHIBIT NEOINTIMAL FORMATION AFTER BALLOON INJURY
C-MET OVEREXPRESSION PROMOTE REENDOTHELIALISATION AND INHIBIT NEOINTIMAL FORMATION AFTER BALLOON INJURY
Objectives
to explore the effect of c-met overexpression in EPCs on reendothelialisation after balloon injury
Me...
Relaxant Effect of Rosuvastatin in Isolated Rat Aorta with Perivascular Adipose Tissue
Relaxant Effect of Rosuvastatin in Isolated Rat Aorta with Perivascular Adipose Tissue
Objective: Rosuvastatin displays favorable pleiotropic effects on vascular system to reduce the risk of cardiovascular events besides providing an intensive reduction in LDL-C leve...
GW24-e3699 Rosuvastatin protects cardiomyocytes from tumour necrosis factor-alpha induced apoptosis via microRNA-210 up-regulation
GW24-e3699 Rosuvastatin protects cardiomyocytes from tumour necrosis factor-alpha induced apoptosis via microRNA-210 up-regulation
Objectives
To investigate the effects of statin, possessed pleiotropic cardioprotective effects, on cardiomyocytes apoptosis induced by TNF-α and the potential me...

