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Monocyte suppressing action of fenofibrate
Bogusław Okopień1, Jan Kowalski, Robert Krysiak
1Department of Clinical Pharmacology, Medical University of Silesia, Medyków 18, PL 40-752 Katowice, Poland. mbkdokop@mp.pl
Pharmacological Reports : PR
|June 30, 2005
Summary
Fenofibrate treatment significantly reduced inflammatory cytokines interleukin 1beta (IL-1beta), interleukin 6 (IL-6), and monocyte chemoattractant protein 1 (MCP-1) in patients with combined hyperlipidemia. This study highlights fenofibrate
Area of Science:
- Cardiovascular Medicine
- Immunology
- Pharmacology
Background:
- Atherosclerosis is an inflammatory disease involving monocytes and pro-inflammatory cytokines.
- Dyslipidemia treatment should address both lipid parameters and inflammation.
- Monocyte-derived cytokines like IL-1beta, IL-6, and MCP-1 are implicated in atherosclerotic plaque development and rupture.
Purpose of the Study:
- To evaluate the effect of fenofibrate, a hypolipidemic drug, on the release of IL-1beta, IL-6, and MCP-1 from monocytes in patients with combined hyperlipidemia (Type IIb).
Main Methods:
- Fourteen patients with Type IIb dyslipidemia resistant to diet were treated with micronized fenofibrate for one month.
- A control group of 12 healthy, age-matched subjects was included.
- Monocytes were isolated before and after treatment, and cytokine release (IL-1beta, IL-6, MCP-1) was measured via ELISA after lipopolysaccharide stimulation.
Main Results:
- Hyperlipidemic patients exhibited significantly higher baseline levels of IL-1beta, IL-6, and MCP-1 compared to controls.
- Fenofibrate treatment for 30 days led to a significant reduction in IL-1beta release (43%), IL-6 release (22%), and MCP-1 release (29%).
Conclusions:
- Patients with Type IIb dyslipidemia show elevated levels of monocyte-derived inflammatory cytokines.
- Fenofibrate therapy effectively inhibits the release of these key inflammatory mediators, suggesting a dual role in managing dyslipidemia and associated inflammation.