Effect of NO on acute severe hepatic injury induced by integrative LPS and GalN
Yuan Ben-li
Abstract
Yuan Ben-li
Abstract
[Objective] Study effect of NO (Nitrogen monoxide) on acute severe hepatic injury induced by integrative LPS (lypopolysacchride) and GalN (D-galactosamine). [Methods] 56 male BALB/c mice were randomly divided into two groups. NS (normal saline, 0.2 mL) was injected intraperitoneally to be regarded as the control group. LPS (5 μg/kg) with GalN (800 mg/kg) together in NS was injected intraperitoneally to be served as the test group. Plasma samples for ALT, AST, NO2- measurements were obtained at 3,6,9 and 12h after respective treatments, meanwhile ISH detection of iNOS mRNA in hepatocyte. [Results] In the test group, the level of ALT, AST, NO2- in plasma was ascending sharply (P 0.01, vs the control group at 12 h). By ISH detection, expression of iNOS mRNA in hepatocyte of liver tissue sections in the test group was enhancing continuously. There were little changes of ALT, AST, NO2- in plasma and expression of iNOS mRNA in iver tissue sections in the control group. [Conlusions] The biosynthetic mechanism of NO is triggered, and NO plays an important role in the acute severe hepatic injury induced by LPS and GalN together. NO may involve in the mechanism of the liver injury.
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[Objective] Study effect of NO (Nitrogen monoxide) on acute severe hepatic injury induced by integrative LPS (lypopolysacchride) and GalN (D-galactosamine). [Methods] 56 male BALB/c mice were randomly divided into two groups. NS (normal saline, 0.2 mL) was injected intraperitoneally to be regarded as the control group. LPS (5 μg/kg) with GalN (800 mg/kg) together in NS was injected intraperitoneally to be served as the test group. Plasma samples for ALT, AST, NO2- measurements were obtained at 3,6,9 and 12h after respective treatments, meanwhile ISH detection of iNOS mRNA in hepatocyte. [Results] In the test group, the level of ALT, AST, NO2- in plasma was ascending sharply (P 0.01, vs the control group at 12 h). By ISH detection, expression of iNOS mRNA in hepatocyte of liver tissue sections in the test group was enhancing continuously. There were little changes of ALT, AST, NO2- in plasma and expression of iNOS mRNA in iver tissue sections in the control group. [Conlusions] The biosynthetic mechanism of NO is triggered, and NO plays an important role in the acute severe hepatic injury induced by LPS and GalN together. NO may involve in the mechanism of the liver injury.
Key concepts: Saline, Hepatocyte, Internal medicine, Messenger RNA, Galactosamine, Endocrinology, Liver injury, Liver tissue