ABSTRACT
Diabetes (type I and type II) affects approximately 13 million people in the United States. Delayed and incomplete healing of wounds can be a major problem for diabetic patients. Macrophages are an important cell in the complex process of wound repair representing the major source of cytokines throughout the wound healing process. Cytokines mediate many of the cellular responses critical to timely wound repair. It has been suggested that diabetes impairs wound healing through disruption of local cytokine production. We previously demonstrated that platelet-derived growth factor B chain (PDGF-B) levels are deficient at the wound site of diabetic rats. In the present study, we measured the levels of several marker cytokines released from cultured peritoneal macrophages of diabetic, nondiabetic hyperlipidemic, and normal rats. The diabetic condition was associated with a generalized reduction of macrophage cytokine release. Nondiabetic hyperlipidemic animals demonstrated similar cytokine reduction supporting the hypothesis that elevated serum lipids are the primary determinants of diabetes-induced reductions in macrophage cytokine release. Thus, manipulation of serum lipids may be a therapeutically useful modality for controlling macrophage cytokine release in the inflammatory and/or wound environment.
Subject(s)
Cytokines/metabolism , Diabetes Mellitus, Experimental/physiopathology , Lipoproteins, LDL/blood , Macrophages, Peritoneal/metabolism , Triglycerides/blood , Animals , Blood Glucose/metabolism , Cells, Cultured , Diabetes Mellitus, Experimental/blood , Diabetes Mellitus, Experimental/metabolism , Enzyme-Linked Immunosorbent Assay , Growth Substances/metabolism , Hyperlipidemias/blood , Hyperlipidemias/metabolism , Hyperlipidemias/physiopathology , Lipopolysaccharides/pharmacology , Macrophages, Peritoneal/drug effects , Male , Rats , Rats, Sprague-Dawley , Stimulation, ChemicalSubject(s)
Alginates/pharmacology , Lymphocyte Activation , Lymphocytes/drug effects , Animals , Cell Adhesion , Cells, Cultured , Fibroblasts/cytology , Fibroblasts/physiology , Humans , Lymphocytes/cytology , Lymphocytes/immunology , Macrophages/cytology , Macrophages/physiology , Mice , Mice, Inbred BALB CABSTRACT
Female Wistar rats were given a single oral dose of aflatoxin B1, either alone or with a large amount of riboflavin. Biochemical and histologic studies were performed for 30 months. Nine animals of 19 in the aflatoxin-treated group and only 5 of 18 in the riboflavin-aflatoxin-treated group developed hepatomas. The number of rats was insufficient for tests of statistical significance to be fruitful. Urinary excretion of tryptophan metabolites was studied in aflatoxin- and riboflavin-treated rats after an oral administration of 10 mg tryptophan/100 g rat. Riboflavin did not affect the percentage of aflatoxin-treated animals with abnormal urinary excretion patterns, but did increase the magnitude of the disturbances in elimination of kynurenic and xanthurenic acids. The hepatic tryptophan-oxygenase activity was increased only in the two groups given riboflavin, and the levels of nucleic acids were the same in all groups.
