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• W1992058051 abstract "Tumor necrosis factor-α (TNF-α) is involved in insulin resistance. Since the fact that peroxisome proliferator-activated receptor γ (PPARγ) ligands inhibit the induction of TNF-α by phorbol ester, but not by lipopolysaccharide (LPS), suggests two pathways to induce TNF-α, we investigated the mechanisms of glycated human albumin (GHA)- or phorbol ester-induced TNF-α in THP-1 cells. GHA induced TNF-α release in differentiated THP-1 cells, while phorbol ester induced TNF-α release in undifferentiated cells but did not induce TNF-α in differentiated cells. Forskolin (adenylate cyclase activator) affected more the GHA-induced TNF-α release than the phorbol 12-myristate 13-acetate (PMA)-induced one in undifferentiated cells. Staurosporine [protein kinase-C (PK-C) inhibitor] and PD98059 [mitogen-activated protein kinase inhibitor (MAPK)] only partially inhibited GHA-induced TNF-α. Catalase completely inhibited GHA-induced TNF-α release; however, superoxide dismutase (SOD) had no effect. These results suggest at least two pathways to induce TNF-α (phorbol ester- and GHA-dependent ways) and that GHA-induced TNF-α release is through predominantly catalase-dependent way in differentiated THP-1 cells." @default.
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• W1992058051 date "2001-05-01" @default.
• W1992058051 modified "2023-10-13" @default.
• W1992058051 title "Tumor necrosis factor-α is induced through phorbol ester- and glycated human albumin-dependent pathway in THP-1 cells" @default.
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• W1992058051 doi "https://doi.org/10.1016/s0898-6568(01)00152-8" @default.
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