Abstract
Selected Compounds Modulate Various Inflammatory Biomarkers in Lipopolysaccharide-Induced Macrophages of PPAR-α Knockout Mice
Highlights
Gene expression results of tumor necrosis factor-α (TNF-α), IL-1β, IL-6, and iNOS activity were consistent with results obtained for TNF-α protein and nitric oxide (NO) production as observed with macrophages of peroxisome proliferator-activated receptor-α (PPAR-α) knockout mice
We have recently described that naturally-occurring compounds play an important therapeutic role in modulating the inflammatory biomarkers in cardiovascular disease, diabetes and cancer [1]
In TG-elicited peritoneal macrophages obtained from peroxisome proliferator activated receptor-α (PPAR-α) knockout female mice, the secretion of TNF-α was activated by some of the compounds rather than inhibited, as compared to control (C57BL/6), and other groups [1]
Summary
We have recently described that naturally-occurring compounds play an important therapeutic role in modulating the inflammatory biomarkers in cardiovascular disease, diabetes and cancer [1]. Those compounds were able to inhibit or activate secretion of TNF-α, and inhibit production of nitric oxide (NO) in murine cell line (RAW264.7), and in lipopolysaccharide-induced thioglycolate (TG)-elicited peritoneal macrophages prepared from C57BL/6 (wild type; control group), BALB/c, double subunits knockout (LMP-7/MECL-1-/-) mice [1]. The important role played by lipopolysaccharides (LPS) in up-regulating inflammation is well-established [2]. We have recently screened several compounds that modulate inflammatory biomarkers (TNF-α, IL-1β, IL-6, and nitric oxide) in response to a variety of stimuli. Our hypothesis is that compounds with those anti-inflammatory properties will be useful for treatment of diabetes, cardiovascular disease, and other diseases based on inflammation
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