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Inhibition of Tumor Necrosis Factor-α Production by DBM1285 through p38 MAPK/ MK-2 Pathway Suppression

The compound DBM1285 effectively suppresses the production of tumor necrosis factor-α (TNF-α) by inhibiting the p38 mitogen-activated protein kinase (MAPK) signaling pathway. In a study involving mouse bone marrow-derived macrophages, pretreatment with various concentrations of BIRB796 revealed significant effects on LPS-induced MK-2 phosphorylation. This research provides insights into the molecular mechanisms underlying anti-inflammatory responses and potential therapeutic strategies for managing inflammatory diseases.

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Inhibition of Tumor Necrosis Factor-α Production by DBM1285 through p38 MAPK/ MK-2 Pathway Suppression

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  1. DBM1285 [cyclopropyl-{4-[4-(4-fluorophenyl)-2-piperidin-4-yl-thiazol-5-yl]pyrimidin-2-yl}amine] suppresses tumor necrosis factor-a production by blocking p38 mitogen-activated protein kinase/mitogen-activated protein kinase-activated protein kinase 2 signaling pathway, Kang JS, Kim HM, Choi IY, Han SB, Yoon YD, Lee H, Park KH, Cho IG, Lee CW, Lee K, Lee KH and Park SK, Journal of Pharmacology and Experimental Therapeutics Supplementary Fig. 3 LPS (1 mg/ml) + BIRB796 (mM) UN VH 0.001 0.01 0.1 1 p-MK-2 MK-2 Effect of BIRB796 on LPS-induced MK-2 phosphorylation in mouse bone marrow-derived macrophages. Mouse bone marrow-derived macrophages were pretreated with vehicle (VH, DMSO) or indicated concentrations of BIRB796 (0.001, 0.01, 0.1 or 1 mM) for 1 h before being incubated with LPS (1 mg/ml) for 30 min. Total cell lysates were prepared and phosphorylated and non-phosphorylated forms of MK-2 was detected by Western immunoblot analysis.

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