[Studies on the role of nitric oxide and tumor necrosis factor in immunological liver injury in mice and effects of new anti-hepatitis compounds on the liver injury].
An immunological liver injury model was established by injection of micro lipopolysaccharide (LPS) into BCG (bacilli Calmette Guéin)-primed mice. It was found that nitric oxide (NO) played dual effects in the liver damage induced by BCG+LPS. The NO coming from phagocytic cells showed toxic effects while those from the other cells displayed beneficial effects. Tumor necrosis factor (TNF) released by macrophages was also implicated to be a key factor in the liver damage induced by BCG + LPS. Kupffer cells were involved in BCG + LPS-induced liver injury by releasing NO and TNF. The mechanism(s) by which the two new hepatoprotectants (SY-801 and SY-640) reduced BCG + LPS-induced liver damage may be through enhancing mouse plasma NO levels and lowering NO production and TNF expression by macrophages.
Wang
G S
GS
Department of Pharmacology, Institute of Materia Medica, Chinese Academy of Medical Sciences, Beijing.
D000818:Animals; D056486:Chemical and Drug Induced Liver Injury / Q000097:blood / Q000188:drug therapy / Q000209:etiology; D007728:Kupffer Cells / Q000378:metabolism; D008070:Lipopolysaccharides; D017737:Macrophages, Peritoneal / Q000378:metabolism; D051379:Mice; D009163:Mycobacterium bovis; D009569:Nitric Oxide / Q000097:blood / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide