Probucol pretreatment enhances the chemotaxis of mouse peritoneal macrophages.

Effects of probucol on cholesterol metabolism in mouse peritoneal macrophages: inhibition of HDL-mediated cholesterol efflux.

Macrophage-derived foam cells are known to play an essential role in the development and progression of atherosclerotic lesions. Probucol prevents oxidative modification of low-density lipoprotein (LDL) and lowers plasma contents of LDL and high-density lipoprotein (HDL). A recent report using apoE -/- mice demonstrated that probucol treatment enhanced atherosclerosis in apoE -/- mice more rapi...

Probucol does not affect lipoprotein metabolism in macrophages of Watanabe heritable hyperlipidemic rabbits.

We recently reported that the antioxidant action of probucol inhibited the progression of atherosclerosis in Watanabe heritable hyperlipidemic (WHHL) rabbits. In this study, we investigated another possible action of probucol: its action as an antiatherogenic agent on macrophages. When WHHL rabbit peritoneal macrophages were pre-incubated in vitro with probucol and then incubated with several a...

Effects of T-2 Toxin on Cytokine Produc-tion by Mice Peritoneal Macrophages and Lymph Node T-Cells

Background: T-2 toxin is a mycotoxin of type A trichothecenes produced by several fungal genera such as Fusarium species. Mycotoxins can affect both cell mediated and humoral immune compartments. Objective: The purpose of this study was to investi-gate the effect of T-2 toxin on cytokine production by mouse peritoneal macrophages and lymph node T cells. Methods: Mouse peritoneal macrophages and...

Peritoneal Macrophages Lipopolysaccharide-Stimulated Mouse Cytokine and Chemokine Production in IL-4 Pretreatment Selectively Enhances

Relative contributions of ABCA1 and SR-BI to cholesterol efflux to serum from fibroblasts and macrophages.

OBJECTIVE Cholesterol efflux is achieved by several mechanisms. This study examines contributions of these pathways to efflux to human serum. METHODS AND RESULTS Human fibroblasts were stably transfected with SR-BI while ABCA1 was upregulated. Quantitation of cholesterol efflux to human serum demonstrated that there was efflux from cells without either protein. Expression of ABCA1 produced a ...