Human C Reactive Protein ELISA Kit (High Sensitivity) (A33007)

Content of protocatechuic acid (PA) in eight locally available fresh fruits was analyzed, and the protective effects of this compound in diabetic mice were examined. PA at 1%, 2%, and 4% was supplied to diabetic mice for 8 weeks. PA treatments significantly lowered plasma glucose and increased insulin levels. PA treatments at 2% and 4% significantly lowered plasminogen activator inhibitor-1 activity and fibrinogen level; increased plasma activity of antithrombin-III and protein C; decreased triglyceride content in plasma, heart, and liver; elevated glutathione level and the retention of glutathione peroxidase and catalase activities in heart and kidney. PA treatments at 2% and 4% also significantly lowered plasma C-reactive protein and von Willebrand factor levels and reduced interleukin-6, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 levels in heart and kidney. These results support that protocatechuic acid could attenuate diabetic complications via its triglyceride-lowering, anticoagulatory, antioxidative, and antiinflammatory effects.

Increasing evidence suggests that the inflammatory biomarker, C-reactive protein (CRP), may play a causal role in the development and progression of atherothrombosis. Since endothelial dysfunction is an early and integral component of atherosclerosis, we hypothesized that endothelial homeostasis would be impaired in CRP-overexpressing CRP transgenic (CRPtg) mice. Male CRPtg and wild-type mice were injected thrice over 2 weeks with vehicle or turpentine to induce the inflammation-sensitive CRP transgene. Serum human CRP levels in turpentine-treated CRPtg mice was 276.28 +/- 95.7 microg/ml. Human CRP was undetectable in the sera of wild-type mice and present at only low levels (1.41 +/- 0.2 microg/ml) in vehicle-treated CRPtg mice (n=6-8 mice/group). Aortic segments from turpentine-induced CRP-overexpressing CRPtg mice demonstrated impaired endothelium-dependent responses to acetylcholine vs. those from vehicle-treated CRPtg controls (57.1 +/- 9.5% vs. 85.0 +/- 5.0%, P<0.05, n=6). Nitric oxide release as well as phosphorylated eNOS protein expression from isolated aortic segments of CRPtg mice overexpressing CRP were markedly reduced compared to that from vehicle-treated controls. Masson's trichrome staining revealed increased perivascular fibrosis in CRP-overexpressing CRPtg mice. CRP overexpression was also associated with augmented aortic endothelial staining for VCAM-1 and MCP-1 and enhanced macrophage infiltration. Mice overexpressing the human CRP gene exhibit endothelial dysfunction, possibly via reduced NO bioavailability, with resultant changes in vascular structure. These data further support a role for CRP in mediating endothelial dysfunction.

Alleviative effects of histidine and carnosine in mice against ethanol-induced oxidative and inflammatory was examined. After chronic alcoholic liver injury was induced, histidine and carnosine at 0.5, 1, 2g/L were added to the drinking water for 3 weeks. Results showed that the post-intake of histidine or carnosine markedly decreased alanine aminotransferase and aspartate aminotransferase activities (P<0.05). Ethanol treatment increased malondialdehyde (MDA) level, decreased glutathione (GSH) content and catalase and glutathione peroxidase (GPX) activities, and increased cytochrome P450 2E1 (CYP2E1) activity in liver (P<0.05). The post-intake of histidine and carnosine significantly decreased MDA formations, increased GSH content, enhanced catalase and GPX activities, and suppressed CYP2E1 activity (P<0.05), in which the effects on catalase and CYP2E1 activities were dose-dependent (P<0.05). Ethanol treatment elevated hepatic levels of c-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) (P<0.05), the post-intake of histidine and carnosine significantly and dose-dependently diminished the release of CRP, IL-6, and TNF-alpha (P<0.05). Ethanol treatment caused down-regulation in both catalase and GPX mRNA expression, and up-regulated both IL-6 and TNF-alpha mRNA expression (P<0.05). Histidine and carnosine post-treatments significantly and dose-dependently upregulated catalase mRNA, and down-regulated mRNA expression of IL-6 and TNF-alpha (P<0.05). Based on the observed anti-oxidative and anti-inflammatory effects, the supplement of histidine or carnosine might be helpful for the treatment of chronic alcoholic liver injury.

Little is known about the relationship between intramyocellular lipid (IMCL) and coronary artery disease (CAD)/non-insulin-dependent diabetes mellitus risk factors. The aim of the study was to examine the relationship between IMCL and CAD/non-insulin-dependent diabetes mellitus risk factors in healthy male (n = 9) and female (n = 10) subjects with similar norm-based aerobic fitness and body composition. Nineteen volunteers (21-36 years) completed health and physical activity questionnaires, cardiovascular and body composition evaluation, and assessment of thigh IMCL using proton magnetic resonance spectroscopy. Outcome measures were blood pressure, total cholesterol, high-density lipoprotein cholesterol, C-reactive protein, interleukin 6, tumor necrosis factor alpha (TNF-alpha), homocysteine, insulin resistance (IR), percentage of body fat, waist-to-hip ratio, physical activity levels, and cardiovascular fitness. Analysis of variance was used for group comparisons. Correlation analyses were used to determine association between variables, and stepwise regression was used to determine predictive variables of IR. Women had 2-fold higher IMCL and greater IR than men (P < .05). Men had greater plasma homocysteine and interleukin 6 concentration (P < .05) as well as stronger correlations with CAD risk factors than female subjects. Correlation analyses using all subjects revealed a significant relationship between IMCL and waist-to-hip ratio, body weight, percentage of body fat, and IR. In the regression analysis, age, IMCL, and TNF-alpha were the strongest predictors of IR (R2 = 0.62, P < .01). Our results suggest that female subjects, matched for age and fitness, have higher IMCL compared with their male counterparts. IMCL was correlated with several CAD and prediabetes markers in both male and female subjects. In the final regression model, age, IMCL, and TNF-alpha were the strongest predictors of IR. Future studies with larger sample sizes are warranted.

OBJECTIVE:

The study involved 25 patients with type-2 hypercholesterolemia (mean age 49.3+/-11.3). The control group consisted of 28 healthy individuals (mean age 50.7+/-7.2).

METHODS:

The cholesterol concentrations in plasma membranes of erythrocytes were measured by means of Liebermann-Burchard reagent. The membrane lipid peroxidation in whole erythrocytes was determined. The membrane fluidity was estimated by spin labelled method.

RESULTS:

The in vitro study shows that the cholesterol concentration in membranes incubated with simvastatin and epicatechin decreases; in healthy donors there are no changes. Simvastatin does not lead to changes in the lipid peroxidation in the in vitro data. Epicatechin decreases the level of membrane lipid peroxidation in patients with hypercholesterolemia and in healthy donors. Simvastatin and epicatechin cause an increase in the fluidity of plasma membranes of erythrocytes.

CONCLUSIONS:

Simvastatin causes the decrease in cholesterol concentration in erythrocytes membranes not only in the in vivo but also the in vitro experiments. Flavonoids have antioxidant properties in vitro. Simvastatin influences the lipid peroxidation only in vivo, not in vitro systems. This observation is an additional contribution to the statins' pleiotropic effect.

BACKGROUND:

Systemic adiponectin is reduced in patients with cardiovascular disease (CVD) and low adiponectin may contribute to the pathogenesis of atherosclerosis. However, circulating adiponectin is elevated in type 1 diabetes (T1D) patients, who have also a higher incidence to develop CVD. Because monocytes play an important role in atherosclerosis, we analysed the influence of adiponectin on cytokine and chemokine release in monocytes from T1D patients and controls.

METHODS:

Systemic adiponectin was determined in the plasma and the high-molecular weight (HMW) form of adiponectin was analysed by immunoblot. Monocytes were isolated from T1D patients and controls and the adiponectin-stimulated release of interleukin-6 (IL-6), monocyte chemotactic protein-1 (MCP-1, CCL2) and interleukin-8 (IL-8, CXCL8) was analysed.

RESULTS:

Systemic adiponectin was higher in T1D patients. Immunoblot analysis of the plasma indicate abundance of HMW adiponectin in T1D patients and controls. IL-6, CCL2 and CXCL8 secretion in response to adiponectin were found induced in monocytes from controls whereas only IL-6 was upregulated in T1D cells. The induction of IL-6 by adiponectin was abrogated by an inhibitor of the NFkappaB pathway.

CONCLUSION:

These data indicate that adiponectin-mediated induction of IL-6, CCL2 and CXCL8 is disturbed in monocytes from T1D patients and therefore elevated systemic adiponectin in T1D patients may be less protective when compared to controls.

BACKGROUND:

Monocytes play an important role in innate immunity and atherosclerosis. A disturbed secretion of cytokines in lipopolysaccharide (LPS) activated monocytes from type 1 diabetes (T1D) patients has been described and may contribute to the impaired inflammatory response in these individuals. In the present study the influence of LPS on five different proteins with a function in immunity and atherosclerosis was analyzed in monocytes from controls and T1D patients.

METHODS:

Monocytes were isolated from controls and T1D patients and the LPS-stimulated increase of IL-6, CXCL8, monocyte chemotactic protein 1 (CCL2, MCP-1) and superoxide dismutase (SOD 2), as well as the LPS-mediated decrease of apolipoprotein E (Apo E) in primary human monocytes from controls and T1D patients was determined.

RESULTS:

CCL2 and IL-6 secretion in response to LPS was found significantly reduced in monocytes from T1D patients when compared to controls whereas basal CCL2 release was similar in control and T1D cells. In contrast, CXCL8 and apolipoprotein E secretion and SOD 2 expression upon LPS stimulation is similar from T1D and control monocytes.

CONCLUSION:

These data indicate that LPS-mediated protein expression is only partly disturbed in monocytes from T1D patients. Reduced secretion of IL-6 and CCL2 in activated monocytes of these patients may contribute to an impaired inflammatory response and vascular disease.