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[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].

Wang Gs

Abstract

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.

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Key concepts: Lipopolysaccharide, Tumor necrosis factor alpha, Nitric oxide, Liver injury, Tumor necrosis factor α, Immunology, Necrosis, Kupffer cell