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Effect of thiol oxidant on tumor necrosis factor α in acute liver injury

Guo Ting-dong

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Abstract

Objective To investigate effect of thiol oxidant on tumor necrosis factorα(TNF-α) in acute liver injury. Methods The acute liver injury model ofmale mice was established by LPS plus D-galactosamine(Galn). Male mice were given diethylmaleate (DEM), a thiol oxidant,ip at the dose of 5 mmol/kg 1 h beforeGaln /LPS. Then the levels of ALT,TNF-α in plasma and GSH in liver were detected. Results Pretreatement with DEM could abrogate the high levels of plasma ALT,TNF-α induced by Galn/LPS. Conclusion Redox manipulation throughthiol oxidation DEM may represent a novel approach to prevent Galn/LPS-inducedacute liver injury by inhibition of TNF-α.

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What this paper is about

Objective To investigate effect of thiol oxidant on tumor necrosis factorα(TNF-α) in acute liver injury. Methods The acute liver injury model ofmale mice was established by LPS plus D-galactosamine(Galn). Male mice were given diethylmaleate (DEM), a thiol oxidant,ip at the dose of 5 mmol/kg 1 h beforeGaln /LPS. Then the levels of ALT,TNF-α in plasma and GSH in liver were detected. Results Pretreatement with DEM could abrogate the high levels of plasma ALT,TNF-α induced by Galn/LPS. Conclusion Redox manipulation throughthiol oxidation DEM may represent a novel approach to prevent Galn/LPS-inducedacute liver injury by inhibition of TNF-α.

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Available abstract

Objective To investigate effect of thiol oxidant on tumor necrosis factorα(TNF-α) in acute liver injury. Methods The acute liver injury model ofmale mice was established by LPS plus D-galactosamine(Galn). Male mice were given diethylmaleate (DEM), a thiol oxidant,ip at the dose of 5 mmol/kg 1 h beforeGaln /LPS. Then the levels of ALT,TNF-α in plasma and GSH in liver were detected. Results Pretreatement with DEM could abrogate the high levels of plasma ALT,TNF-α induced by Galn/LPS. Conclusion Redox manipulation throughthiol oxidation DEM may represent a novel approach to prevent Galn/LPS-inducedacute liver injury by inhibition of TNF-α.

Key concepts: Tumor necrosis factor alpha, Thiol, Glutathione, Liver injury, Necrosis, Medicine, Tumor necrosis factor α, Pharmacology

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