Biomedical subjects

Zbigniew S Herman

Publications and source records attributed to Zbigniew S Herman.

23 records · Page 2Linked to original sources

PubMedDate not supplied

Monocyte suppressing action of fenofibrate.

Since atherosclerosis has been proven to be an inflammatory disease, it is obvious that the proper treatment for dyslipidemia should not only correct lipid parameters but also inhibit inflammation. Monocytes and monocyte-derived proinflammatory cytokines are widely known to be involved in the formation and rupture of the atherosclerotic plaque. The aim of our study was to assess the effect of fenofibrate, a commonly used hypolipidemic drug, on the release of interleukin 1beta (IL-1beta), interleukin 6 (IL-6) and monocyte chemoattractant protein 1 (MCP-1) by monocytes from patients with combined hyperlipidemia. Fourteen patients with biochemically confirmed type IIb dyslipidemia who did not respond to a low-fat diet were treated with micronized fenofibrate for 1 month. The control group included 12 healthy, normolipidemic, age-matched subjects. To accurately evaluate the levels of the inflammatory cytokines, we excluded patients with any inflammatory disease. Monocytes were isolated from peripheral blood before and after the treatment. IL-1beta, IL-6 and MCP-1 release was measured by enzyme-linked immunosorbent assay (ELISA) after lipopolysaccharide stimulation. IL-1beta, IL-6 and MCP-1 levels were significantly higher in hyperlipidemic patients compared to the control (143.9 +/- 6.5 vs. 74.4 +/- 4.4 pg/ml; 8212 +/- 285 vs. 6110 +/- 170 pg/ml; 19.6 +/- 0.9 vs. 12.3 +/- 0.6 ng/ml, respectively). Thirty-day fenofibrate treatment decreased the release of IL-1beta by 43% (143.9 +/- 6.5 vs. 86.2 +/- 5.9 pg/ml), of IL-6 by 22% (8212 +/- 285 vs. 6330 +/- 234 pg/ml), and of MCP-1 by 29% (19.6 +/- 0.9 vs. 14.0 +/- 0.8 ng/ml). The evaluated cytokines were markedly elevated in patients with type IIb dyslipidemia. Effective fenofibrate therapy had a significant inhibitory effect on the release of monocyte-derived inflammatory cytokines.

Adult↗

PubMedDate not supplied

[Antidepressants and cytokines--clinical and experimental studies].

Clinical and experimental studies indicate that stress and depression are associated with the up-regulation of the immune system, including increased production of pro-inflammatory cytokines. When administered to patients or laboratory animals, some of these cytokines induce typical symptoms of depression. It is known that cytokines modulate brain neurotransmission and the activity of the hypothalamic-pituitary-adrenal axis, both of which are disturbed in depression. This review summarizes in vivo, ex vivo and in vitro clinical and experimental studies of the effect of antidepressants on cytokine production. In vitro culture and animal studies in particular suggest that antidepressants of several classes decrease the production of pro-inflammatory cytokines and shift the pro/anti-inflammatory cytokine balance towards the latter. Some studies suggest that immunological disturbances, including changes in cytokine levels, are not shared by all depressive patients, which means that only in certain groups of patients may the immunomodulatory action of antidepressants play a significant role in producing the therapeutic effect.

Animals↗

PubMedDate not supplied

Lack of effect of some dopamine and non-dopamine receptor ligands on amphetamine-induced changes in the rat brain neuropeptide Y system.

None of the receptor ligands studied: the dopamine D2 antagonist eticlopride, D2/D3 antagonist haloperidol, alpha1-adrenergic antagonist prazosin, N-methyl-D-aspartate antagonist MK-801, 5-HT2/D2 antagonist mianserin, D2/D3 agonist quinpirole and alpha2-adrenergic agonist clonidine co-administrated with repeated amphetamine (AMPH) injections blocked the AMPH-induced decrease in the striatal and nucleus accumbens neuropeptide Y (NPY) levels. Only the D1/D5 receptor antagonist SCH 23390 insignificantly attenuated this effect what suggests that these dopamine receptor subtypes may partially mediate AMPH effect on NPY. Moreover, the results of multiple administrations of the receptor ligands to control rats indicate that the NPY systems in both structures under study are modulated in the same manner by dopaminergic activity and differentially by adrenergic, N-methyl-D-aspartate and serotonergic activity.

Adrenergic alpha-Agonists↗

PubMedDate not supplied

Plasma concentrations of adhesion molecules and chemokines in patients with essential hypertension.

Arterial hypertension vascular injury results in serious complications, such as left-ventricular hypertrophy and myocardial failure, ischemic heart disease and cerebral stroke. Currently, it is well known that inflammatory factors play a significant role in the mechanisms that trigger and enhance the remodeling of the vascular wall. A number of data suggest an important role of adhesion molecules and chemokines in this processes. The aim of this study was measuring the plasma levels of soluble Intercellular Adhesion Molecule 1 (sICAM-1) and Monocyte Chemoattractant Peptide1 (MCP-1) in patients with essential hypertension vs. healthy volunteers by ELISA method (R&D kits). sICAM-1 and MCP-1 levels were significantly higher in hypertensive patients compared to controls (sICAM-1: 279.2 +/- 8.8 ng/ml vs. 224.4 +/- 1.8 ng/ml; p < 0.001; MCP-1: 142.2 +/- 7 pg/ml vs. 95.4 +/- 36 pg/ml; p < 0.0001. Our results indicate that arterial hypertension alone (without inflammation, lipid and carbohydrate disorders) may increase the expression of these cytokines and contribute to the progression of endothelial injury.

Adult↗

PubMedDate not supplied

Extralipid effects of micronized fenofibrate in dyslipidemic patients.

The aim of this study was to evaluate the levels of lipid and extralipid parameters in patients with atherogenic dyslipidemia. We investigated the lipid-lowering therapeutic efficacy of fenofibrate and its extralipid influence on oxidized low-density lipoprotein (oxLDL), C-reactive protein (CRP), Fibrinogen, factor VII and plasminogen activator type 1 (PAI-1) during 1-month treatment. Fourteen individuals with HLPIIb were treated with micronized fenofibrate (267 mg/d) for 1 month. The control group included twelve volunteers. Lipidograms were determined with enzymatic kits. ELISA method was used to measure oxLDL and PAI-1. Plasma CRP levels were measured spectrophotometrically. Fibrinogen and factor VII serum levels were evaluated with automatic coagulometer. After 1-month therapy with micronized fenofibrate, we observed a significant reduction of total cholesterol (TC) (277.2 to 217.8 mg/dl, p < 0.05), LDL (183.6 to 129.4 mg/dl, p < 0.05), trigliceryde (TG) (316.7 to 220.6 mg/dl, p < 0.05), oxLDL (68.7 +/- 5.5 to 39.7 +/- 3.7 U/l, p < 0.001) and increase in high-density lipoprotein (HDL) (35.1 to 41.9 mg/dl, p < 0.05). Fibrate treatment also decreased CRP(5.81 +/- 0.26 to 5.08 +/- 0.06 mg/l, p < 0.001), PAI-1 (120.4 +/- 9.7 to 84.7 +/- 5.9 ng/ml; p < 0.05), fibrinogen (3.65 +/- 0.17 to 3.44 +/- 0.16 g/l, ns) and factor VII (159.7% +/- 56.7 to 141% +/- 42.4, ns). The micronized fenofibrate at a daily dose of 267 mg demonstrated a highly beneficial effect on all lipid parameters and advantageous influence on inflammatory and thrombogenic plasma risk factors in patients with dyslipidemia HLPIIb.

Adult↗