期刊
JOURNAL OF LABORATORY AND CLINICAL MEDICINE
卷 135, 期 5, 页码 387-395出版社
MOSBY-YEAR BOOK INC
DOI: 10.1067/mlc.2000.106451
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资金
- NIAAA NIH HHS [1K20AA00190-01, 1K21 AA00205-01] Funding Source: Medline
- NINDS NIH HHS [1PO1 NS31220-01A1] Funding Source: Medline
Increased tumor necrosis factor-a activity has been reported in patients with alcoholic hepatitis and is implicated in its pathogenesis. The aim of this study was to investigate potential mechanisms of increased tumor necrosis factor-a activity in alcoholic hepatitis. Monocyte nuclear factor-kb activity was assessed by electrophoretic mobility shift assay, monocyte tumor necrosis factor-a mRNA was semiquantitatively assessed by reverse transcriptase polymerase chain reaction, and tumor necrosis factor-a in monocyte culture supernatants was measured. There was significantly greater spontaneous nuclear factor-kB activity in the monocytes of 6 patients with alcoholic hepatitis as compared with that in the monocytes of control subjects. There was spontaneous tumor necrosis factor-a mRNA and tumor necrosis factor-a release from the monocytes of patients with alcoholic hepatitis but not from the monocytes of normal subjects. Endotoxin increased nuclear factor-kB activity and induced tumor necrosis factor-a mRNA and tumor necrosis factor-a release from normal subjects' monocytes, Endotoxin further increased nuclear factor-ks activity, tumor necrosis factor-a mRNA, and tumor necrosis factor-a release from the monocytes of patients with alcoholic hepatitis. Supershift assays indicate that the monocyte nuclear factor-kB activation involves the p50 and p65 subunits, Dysregulated tumor necrosis factor-a metabolism in alcoholic hepatitis monocytes is associated with increased nuclear factor-kB activity and tumor necrosis factor-a mRNA expression.
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