Inflammation is increased by infection with pathogens such as viruses, bacteria, and parasites. High levels of inflammatory mediators and infiltration of macrophages into inflammatory lesions were reported in severe inflammatory diseases. Here, the aim of this study was to evaluate an anti-inflammatory activity of di-2-pyridylketone-4,4-dimethyl-3-thiosemicarbazone (Dp44mT) on lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. Dp44mT (1–100 ng/mL) had no effect on viability of RAW 264.7 macrophages. Dp44mT (100 ng/mL) significantly reduced LPS-induced release of nitric oxide and expression of inducible nitric oxide synthase and cyclooxygenase-2. A significant upregulation of tumor necrosis factor (TNF)-α and interleukin (IL)-6 by LPS stimulation was downregulated by treatment with Dp44mT. Dp44mT blocked activation of nuclear factor-κB by the interruption of IκBα phosphorylation. Dp44mT suppressed the phagocytosis. Furthermore, administration of Dp44mT significantly reduced the serum levels of TNF-α and IL-6 in LPS-treated mice without side effects. In conclusion, these results indicate that Dp44mT has an anti-inflammatory activity and may be of therapeutic significant for the prevention and treatment of inflammatory diseases.

感染病原体如病毒、细菌和寄生虫会增加炎症。据报道，在严重的炎症性疾病中，炎症介质水平高，巨噬细胞浸润炎症病变。在这里，本研究的目的是评估 di-2-pyridylketone-4,4-dimethyl-3-thiosemicarbazone (Dp44mT) 对脂多糖 (LPS) 刺激的 RAW 264.7 巨噬细胞的抗炎活性。Dp44mT (1–100 ng/mL) 对 RAW 264.7 巨噬细胞的活力没有影响。Dp44mT (100 ng/mL) 显着降低 LPS 诱导的一氧化氮释放和诱导型一氧化氮合酶和环氧合酶-2 的表达。通过用 Dp44mT 处理，LPS 刺激对肿瘤坏死因子 (TNF)-α 和白细胞介素 (IL)-6 的显着上调被下调。Dp44mT 通过中断 IκBα 磷酸化来阻断核因子-κB 的激活。Dp44mT 抑制吞噬作用。此外，Dp44mT 的给药显着降低了 LPS 治疗小鼠的血清 TNF-α 和 IL-6 水平，而没有副作用。总之，这些结果表明 Dp44mT 具有抗炎活性，可能对炎症性疾病的预防和治疗具有治疗意义。