The aim of the present study was to investigate the effects of 5-bromo-2-hydroxy-4-methyl-benzaldehyde (BHMB) on inflammatory responses to lipopolysaccharide (LPS) in RAW 264.7 cells and the associated mechanism of action. BHMB concentration-dependently suppressed protein and mRNA expressions of iNOS and COX-2, thereby inhibiting the production of NO and PGE₂ in LPS-stimulated RAW 264.7 cells. BHMB also reduced the mRNA expression of TNF-α, IL-6, and IL-1β in LPS-stimulated RAW 264.7 cells. To elucidate the mechanism underlying the anti-inflammatory activity of BHMB, we investigated the effects of BHMB on the mitogen-activated protein kinase and nuclear factor-kappa B (NF-κB) pathways. BHMB suppressed the phosphorylation and degradation of IκB-α and markedly inhibited the nuclear translocation of p65 and p50 in LPS-stimulated RAW 264.7 cells. The compound also inhibited the LPS-stimulated phosphorylation of ERK and p38. Taken together, these results illustrated that BHMB suppresses pro-inflammatory mediator and cytokine expression in LPS-stimulated RAW 264.7 cells by inhibiting the phosphorylation of ERK and p38 and the activation of NF-κB.

本研究的目的是研究5-溴-2-羟基-4-甲基-4-苯甲醛（BHMB）对RAW 264.7细胞对脂多糖（LPS）的炎症反应的作用及其相关的作用机制。BHMB浓度依赖性地抑制iNOS和COX-2的蛋白质和mRNA表达，从而抑制NO和PGE _2的产生在LPS刺激的RAW 264.7细胞中。BHMB还降低了LPS刺激的RAW 264.7细胞中TNF-α，IL-6和IL-1β的mRNA表达。为了阐明BHMB抗炎活性的潜在机制，我们研究了BHMB对有丝分裂原激活的蛋白激酶和核因子-κB（NF-κB）途径的影响。BHMB抑制LPS刺激的RAW 264.7细胞中IκB-α的磷酸化和降解，并显着抑制p65和p50的核易位。该化合物还抑制LPS刺激的ERK和p38磷酸化。综上所述，这些结果说明，BHMB通过抑制ERK和p38的磷酸化以及NF-κB的活化来抑制LPS刺激的RAW 264.7细胞中促炎性介质和细胞因子的表达。