The objective of this study was to investigate the anti-inflammatory effect of chlorogenic acid methyl ester (CME) and the molecular mechanism involved, through using non-infectious inflammation and infectious inflammation animal models as well as lipopolysaccharide (LPS)-stimulated mouse macrophage RAW264.7 cell models. Our results demonstrated that CME markedly inhibited ear swelling, paw swelling and granuloma swelling, and decreased intraperitoneal capillary permeability in non-infectious inflammation. Moreover, CME significantly alleviated the pathological damage of the lung tissue, reduced the levels of PGE2 and IL-1β in the serum and the protein expression levels of related-inflammatory factors in the lung tissue of LPS-induced mice with acute lung injury (ALI). In addition, CME affected the RAW264.7 cell cycle and inhibited the protein expressions of COX-2 and NLRP3 and prevented the phosphorylation of NF-κB p65 in RAW264.7 cells treated with LPS. These observations not only validated the anti-inflammatory effects of CME, but also revealed the underlying molecular basis, which involves the down-regulation of the expression of inflammatory factors and blockade of the COX-2/NLRP3/NF-κB signaling pathway.

中文翻译：

---

绿原酸甲酯通过抑制COX-2 / NLRP3 /NF-κB途径 发挥强大的抗炎作用

这项研究的目的是通过使用非传染性炎症和传染性炎症动物模型以及脂多糖（LPS）刺激的小鼠巨噬细胞RAW264，研究绿原酸甲酯（CME）的抗炎作用及其涉及的分子机制。 .7单元模型。我们的结果表明，CME在非感染性炎症中显着抑制了耳部肿胀，爪部肿胀和肉芽肿肿胀，并降低了腹膜内毛细血管通透性。此外，CME显着减轻了肺组织的病理损伤，降低了血清中PGE2和IL-1β的水平以及LPS诱导的急性肺损伤小鼠（ALI）肺组织中相关炎症因子的蛋白表达水平）。此外，CME影响了RAW264。LPS处理的RAW264.7细胞具有7个细胞周期并抑制COX-2和NLRP3的蛋白表达，并阻止NF-κBp65的磷酸化。这些观察结果不仅验证了CME的抗炎作用，而且揭示了潜在的分子基础，这涉及炎性因子表达的下调和COX-2 / NLRP3 /NF-κB信号通路的阻断。