Evidence on Inducible Nitric Oxide Synthase Induction in Subjects with Fulminant Hepatic Failures
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〔背景〕急性肝不全においては,サイトカインカスケードが活性化されることにより, iNOSが誘導されて一酸化窒素(NO)産生が増加すると考えられる.本論文では,急性肝不全におけるNOの役割を検討するため, iNOSおよびiNOS mRNAの発現と分布に関して検討した.〔方法〕急性肝不全患者と正常人各5名の血清中NO代謝産物濃度をグリス法により測定した.また, 14名の急性肝不全患者から得た肝組織標本について, NOに関しては免疫染色法, iNOSとmRNAに関してはWestern blot法とin situ hybridizationにより検討した. 〔結果〕血清NO代謝産物濃度は,急性肝不全患者で101.6±24.3μmol/L,正常人で23.4±4.2μmol/Lであり,急性肝不全患者において有意に高かった. iNOSは免疫組織学的に正常肝標本には見出すことができなかったが,急性肝不全患者から得られた肝組織標本においては大部分で検出された. iNOS mRNAについても急性肝不全患者の肝細胞とクッパー細胞において増加していた.しかし,正常肝標本には発現していなかった.〔結論〕急性肝不全においては, iNOSによりNO産生が増大し,そのことが発症に大きく関わっていると考えられた.Background In the present study, we analyzed the increase in nitric oxide (NO) production due to inducible nitric oxide synthase (iNOS) induction that resulted from the activation of a cytokine cascade in subjects with fulminant hepatic failures (FHF). Methods The serum levels of NO metabolites assayed by the Griess reaction in FHF patients and normal subjects were compared. The presence of NO in the liver was examined by immunostaining, together with a study of the level of expression of iNOS and its mRNA by Western blot analysis and in situ hybridization. Results The mean serum levels of NO metabolites were 101.6±24.3μmol/L in patients with FHF and 23.4±4.2μmol/L in normal subjects (p<0.01). Western blotting detected iNOS, and immunostaining revealed this protein in almost all the cells in the liver specimens obtained from the FHF cases. iNOS mRNA expression was also increased in the hepatocytes and Kupffer cells in liver specimens obtained from cases of FHF. The increases in iNOS protein and mRNA expressions reflect increased NO synthesis. Conclusions Increased NO production by iNOS may potentially play a role in the pathogenesis of FHF.
- 東京女子医科大学学会の論文
- 2004-11-25
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