Diazepam effects on peritoneal macrophage activity and corticosterone serum levels in balb/c mice

• Published in: Life sciences (1973) Vol. 65; no. 20; pp. 2157 - 2165
• Main Authors: Massoco, C.O., Palermo-Neto, J.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 1999
• Subjects: Administration, Oral; Animals; Anti-Anxiety Agents - pharmacology; Cell Migration Inhibition; Cell Movement - drug effects; Cell Movement - physiology; Cells, Cultured; Corticosterone - blood; diazepam; Diazepam - pharmacology; Hydrogen Peroxide - metabolism; immune system; Macrophage Activation - drug effects; macrophage H 2O 2 release; macrophage phagocytosis; macrophage spreading; Macrophages, Peritoneal - drug effects; Macrophages, Peritoneal - physiology; Male; Mice; Mice, Inbred BALB C; Phagocytosis - drug effects; Phagocytosis - physiology; Tetradecanoylphorbol Acetate - pharmacology; macrophage phagocytosis; immune system; diazepam; macrophage H 2O 2 release; macrophage spreading
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/S0024-3205(99)00481-6

In the present experiment we investigate the effects of diazepam on macrophage activity and serum corticosterone levels in mice. Adult mice were treated with diazepam (1.5 mg/kg — group E) or with control solution (group C 1) for 7 days; some animals were only handled, receiving no treatment (group C 2). Oral onco-BCG was used for peritoneal macrophage activation. Diazepam treatment: 1- decreased macrophage spreading and phagocytosis; 2-decreased the concentrations of H 2O 2 spontaneously but not phorbol myristateacetate-induced release. In relation to mice of group C 1, diazepam treatment increased the serum levels of corticosterone. No differences were detected between data of groups C 1 and C 2 both for macrophage activity and serum corticosterone levels. The present data were explained on the basis of a synergistically action for diazepam through peripheral type binding sites (PBR) present in both adrenals and macrophages, stimulating adrenal glucocorticoid production and altering the macrophage cytokine network.