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- W2395179140 abstract "Background : The induction of production and production inhibition of 1-antichymotrypsin (ACT), IL-1, IL-1 receptor and macrophage inflammatory protein-1 (MIP-1) receptor in A1-42 (A)-stimulated U373MG cell, the human astrocytoma cell line, have never been reported. Methods : U373MG cells (110 cells in RPMI-1640 media) were incubated for overnight after administration of a single dose of 20 M of Aor 0.5 ng/ml of TNFor both. Actinomycin D (2.5 M) or cycloheximide (2.5 M) was also added to the cell suspension. Messenger RNA expression of ACT, IL-1, IL-1receptor and MIP-1 receptor was measured by RT-PCR. Western blot was done and nitrocellulose paper was stained with anti-ACT and anti-GFAP antibody. NF B activation after treatment of Ain U373MG cells was detected by electrophoretic mobility-shift assay. Results : Aand TNFboth increased production of ACT in a dosedependent manner. TNFenhanced A-induced mRNA had increases of ACT, IL-1, IL-1receptor and MIP-1 receptor. Activated NF B was demonstrated in the A, TNF-stimulated U373MG cells. Actinomycin suppresses mRNA level of ACT and IL-1receptor but cycloheximide inhibits the expression of ACT, IL-1and MIP-1receptor. Conclusions : TNFincreases synthesis of ACT, IL-1, IL-1receptor and MIP-receptor in A-stimulated astrocyte, which, as a result, may contribute to the neuroinflammation of Alzheimer's disease." @default.
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- W2395179140 date "2002-01-01" @default.
- W2395179140 modified "2023-09-28" @default.
- W2395179140 title "Induction of Various Pro-inflammatory Mediators and Their Receptors in Human Astrocytoma Cell Line Stimulated by $beta$-amyloid Protein" @default.
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