PDF(Pubmed)
Abstract：
UNASSIGNED: Atherosclerosis, a leading cause of global cardiovascular mortality, is characterized by chronic inflammation. Central to this process is the NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome, which significantly influences atherosclerotic progression. Recent research has identified that the olfactory receptor 2 (Olfr2) in vascular macrophages is instrumental in driving atherosclerosis through NLRP3- dependent IL-1 production.
UNASSIGNED: To investigate the effects of Corilagin, noted for its anti-inflammatory attributes, on atherosclerotic development and the Olfr2 signaling pathway, our study employed an atherosclerosis model in ApoE-/- mice, fed a high-fat, high-cholesterol diet, alongside cellular models in Ana-1 cells and mouse bone marrow-derived macrophages, stimulated with lipopolysaccharides and oxidized low-density lipoprotein.
UNASSIGNED: The vivo and vitro experiments indicated that Corilagin could effectively reduce serum lipid levels, alleviate aortic pathological changes, and decrease intimal lipid deposition. Additionally, as results showed, Corilagin was able to cut down expressions of molecules associated with the Olfr2 signaling pathway.
UNASSIGNED: Our findings indicated that Corilagin effectively inhibited NLRP3 inflammasome activation, consequently diminishing inflammation, macrophage polarization, and pyroptosis in the mouse aorta and cellular models via the Olfr2 pathway. This suggests a novel therapeutic mechanism of Corilagin in the treatment of atherosclerosis.
UNASSIGNED: To investigate the effects of Corilagin, noted for its anti-inflammatory attributes, on atherosclerotic development and the Olfr2 signaling pathway, our study employed an atherosclerosis model in ApoE-/- mice, fed a high-fat, high-cholesterol diet, alongside cellular models in Ana-1 cells and mouse bone marrow-derived macrophages, stimulated with lipopolysaccharides and oxidized low-density lipoprotein.
UNASSIGNED: The vivo and vitro experiments indicated that Corilagin could effectively reduce serum lipid levels, alleviate aortic pathological changes, and decrease intimal lipid deposition. Additionally, as results showed, Corilagin was able to cut down expressions of molecules associated with the Olfr2 signaling pathway.
UNASSIGNED: Our findings indicated that Corilagin effectively inhibited NLRP3 inflammasome activation, consequently diminishing inflammation, macrophage polarization, and pyroptosis in the mouse aorta and cellular models via the Olfr2 pathway. This suggests a novel therapeutic mechanism of Corilagin in the treatment of atherosclerosis.
摘要：
■动脉粥样硬化，全球心血管死亡的主要原因，以慢性炎症为特征。这个过程的核心是含NOD样受体pyrin结构域3（NLRP3）炎性体，显著影响动脉粥样硬化进展。最近的研究已经确定，血管巨噬细胞中的嗅觉受体2（Olfr2）通过NLRP3依赖性IL-1的产生来驱动动脉粥样硬化。
■为了研究Corilagin的作用，以其抗炎特性而闻名，关于动脉粥样硬化发展和OlfR2信号通路，我们的研究采用了ApoE-/-小鼠的动脉粥样硬化模型，喂高脂肪，高胆固醇饮食,与Ana-1细胞和小鼠骨髓源性巨噬细胞的细胞模型一起，用脂多糖和氧化低密度脂蛋白刺激。
■体内和体外实验表明，Corilagin可以有效降低血脂水平，缓解主动脉病理变化，减少内膜脂质沉积。此外,如结果显示，Corilagin能够降低与Olfr2信号通路相关的分子的表达。
■我们的研究结果表明，Corilagin能有效抑制NLRP3炎性体的激活，因此减少炎症，巨噬细胞极化，和通过Olfr2途径在小鼠主动脉和细胞模型中的焦亡。这提示了Corilagin治疗动脉粥样硬化的新治疗机制。
■为了研究Corilagin的作用，以其抗炎特性而闻名，关于动脉粥样硬化发展和OlfR2信号通路，我们的研究采用了ApoE-/-小鼠的动脉粥样硬化模型，喂高脂肪，高胆固醇饮食,与Ana-1细胞和小鼠骨髓源性巨噬细胞的细胞模型一起，用脂多糖和氧化低密度脂蛋白刺激。
■体内和体外实验表明，Corilagin可以有效降低血脂水平，缓解主动脉病理变化，减少内膜脂质沉积。此外,如结果显示，Corilagin能够降低与Olfr2信号通路相关的分子的表达。
■我们的研究结果表明，Corilagin能有效抑制NLRP3炎性体的激活，因此减少炎症，巨噬细胞极化，和通过Olfr2途径在小鼠主动脉和细胞模型中的焦亡。这提示了Corilagin治疗动脉粥样硬化的新治疗机制。
