The excessive or prolonged production of inflammatory mediators can result in numerous chronic diseases, such as rheumatoid arthritis, atherosclerosis, diabetes, and cancer. Therefore, for many inflammatory-related diseases, pharmaceutical intervention is required to restrain the excessive release of such inflammatory mediators. Novel therapeutics and mechanistic insight are sought for the management of chronic inflammatory diseases. Resokaempferol (RES) is a type of flavonoid recently reported to demonstrate anti-cancer properties. However, the anti-inflammatory capacity of RES has not been studied to date. Therefore, this study investigated whether RES is capable of suppressing the inflammatory response to lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and the mechanism by which this is achieved. We found that RES attenuated the LPS-induced production of nitric oxide (NO), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), monocyte chemotactic protein 1 (MCP-1) and IL-6. RES also inhibited the nuclear translocation of signal transducer and activator of transcription (STAT) 3 and reduced the LPS-mediated phosphorylation of Janus kinase (JAK) 2 and STAT3 at the sites of Ser727 and Tyr705. RES also inhibited the activation of NF-κB and JNK/p38 MAPK signaling pathways in LPS-induced RAW264.7 cells. Additionally, RES inhibited the activation of the JAK2/STAT3 pathway in exogenous IL-6-activated RAW264.7 macrophages. We conclude that RES inhibits the inflammatory response in activated macrophages by blocking the activation of the JAK2/STAT3 pathway by both LPS and IL-6 signaling.

炎性介质的过量或长时间产生可导致许多慢性疾病，例如类风湿性关节炎，动脉粥样硬化，糖尿病和癌症。因此，对于许多炎性相关疾病，需要药物干预以抑制此类炎性介质的过度释放。正在寻求用于慢性炎症性疾病治疗的新颖疗法和机理见解。Resokaempferol（RES）是一种类黄酮，最近被报道具有抗癌作用。然而，迄今为止尚未研究RES的抗炎能力。因此，本研究调查了RES是否能够抑制对脂多糖（LPS）刺激的RAW264.7巨噬细胞的炎症反应，以及其实现的机制。我们发现RES减弱了LPS诱导的一氧化氮（NO），诱导型一氧化氮合酶（iNOS），环氧化酶2（COX-2），前列腺素E2（PGE2），白介素（IL）-1β，肿瘤坏死因子的产生-α（TNF-α），单核细胞趋化蛋白1（MCP-1）和IL-6。RES还抑制了信号转导子和转录激活子（STAT）3的核易位，并减少了Ser727和Tyr705处LPS介导的Janus激酶（JAK）2和STAT3的磷酸化。RES还抑制LPS诱导的RAW264.7细胞中NF-κB和JNK / p38 MAPK信号通路的激活。此外，RES抑制了外源IL-6激活的RAW264.7巨噬细胞中JAK2 / STAT3途径的激活。