Metformin inhibits nuclear factor kappaB activation and decreases serum high-sensitivity C-reactive protein level in experimental atherogenesis of rabbits.

Previous studies demonstrated that metformin has obvious antiatherogenic properties, but the exact mechanism remains unclear. Therefore, we established an atherosclerotic rabbit model in order to investigate the potential effects of metformin on transcription factor nuclear factor kappaB (NF-kappaB) and serum high-sensitivity C-reactive protein (hs-CRP) level, which had been regarded as proatherogenic factors. New Zealand rabbits were randomly divided into three groups: a control group (n = 8), an atherosclerotic group (AS group, n = 8), and a metformin treatment group (Met group, n = 8).

Antiapoptosis and mitochondrial effect of pioglitazone preconditioning in the ischemic/reperfused heart of rat.

Purpose: Pioglitazone, used clinically in the treatment of type 2 diabetes mellitus, has been implicated as a regulator of cellular inflammatory and ischemic responses. The present study examined whether pioglitazone could inhibit cardiomyocyte apoptosis and reduce mitochondrial ultrastructure injury and membrane potential loss in the ischemic/reperfused heart of the rat. Furthermore, we investigated whether the protective effect of pioglitazone was related to opening of the mitochondrialATP-sensitive potassium channels.

Folic acid reduces chemokine MCP-1 release and expression in rats with hyperhomocystinemia.

Objective: This study aimed to investigate the effects of folate on the monocyte chemoattractant protein-1 (MCP-1) expression and release in rats with hyperhomocystinemia induced by ingestion of excess methionine.

Methods And Results: Thirty male Sprague-Dawley rats (200+/-20 g) were randomly divided into three groups (n=10 for each group): control group (Control), high-homocystinemia (Hhcy) group, and folate treatment (FA) group. They were fed with a normal regular diet, enriched by 1.

Role of norepinephrine in development of short-term myocardial hibernation.

Aim: To investigate the role of norepinephrine in the development of short-term myocardial hibernation.

Methods: Hearts were removed from rats and set up as isometrically beating or short-term hibernation models. The hearts were perfused with modified Krebs-Henseleit buffer under a controlled perfusion pressure.

Folic acid reduces adhesion molecules VCAM-1 expession in aortic of rats with hyperhomocysteinemia.

To investigate effects of supplementation of folic acid on the expression of adhesion molecules VCAM-1 in the aortas of rats with hyperhomocysteinemia. Thirty male SD rats (200 +/- 20 g) were invided into 3 groups (n = 10 for each group): control group(Control), high Met group(Met) and Met plus Folate group(Met + Folate), fed. for 45 days.

[Effects of atorvastatin on the function of dendritic cells in patients with unstable angina pectoris].

Objective: To investigate the function of dendritic cells (DC) in patients with unstable angina pectoris (UAP) and the effects of atorvastatin on it.

Methods: 27 patients with UAP were divided into two groups treated respectively with regular pharmacotherapy and regular pharmacotherapy plus atorvastatin. PBMC from the UAP patients (before and 2 weeks after the treatment) and 11 healthy subjects were incubated and induced to mature DC in a completed medium containing GM-CSF and IL-4.

[The relationship between gap junctional remodeling and atrial fibrillation in patients with rheumatic heart disease].

Objective: To investigate the relationship between the alternations in the expression and distribution of connexin 40 (Cx40) and connexin 43 (Cx43) and atrial fibrillation (AF) in patients with rheumatic heart disease.

Methods: Biopsy was conducted to take specimens of right atrial appendage (RAA) from 32 patients with rheumatic heart disease, 21 with AF and 11 with sinus rhythm (SR) during valve replacement. The protein levels of Cx40 and Cx43 were examined by immunoconfocal microscopy and Western blotting.

[Adenosine protects cardiomyocytes from hypoxia/reoxygenation injury].

The aim of this study was to investigate the protective effect of adenosine (ADO) on cardiomyocytes following hypoxia/reoxygenation (H/R) and its molecular mechanism. Primary cultured cardiomyocytes of neonatal rats were divided into two groups, namely H/R (control) and ADO (1.0 micromol/L) groups.