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- Title
Corilagin alleviates atherosclerosis by inhibiting NLRP3 inflammasome activation via the Olfr2 signaling pathway in vitro and in vivo.
- Authors
Jinqian Mao; Yunfei Chen; Qiushuo Zong; Cuiling Liu; Jiao Xie; Yujie Wang; Fisher, David; Nguyen Thi Thu Hien; Pronyuk, Khrystyna; Musabaev, Erkin; Yiqing Li; Lei Zhao; Yiping Dang
- Abstract
Introduction: Atherosclerosis, a leading cause of global cardiovascularmortality, 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. Methods: 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, highcholesterol diet, alongside cellular models in Ana-1 cells and mouse bone marrow-derived macrophages, stimulated with lipopolysaccharides and oxidized low-density lipoprotein. Results: 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. Discussion: 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 therapeuticmechanism of Corilagin in the treatment of atherosclerosis.
- Subjects
ELLAGITANNINS; NLRP3 protein; CELLULAR signal transduction; INFLAMMASOMES; ATHEROSCLEROSIS; HYDROXYCHOLESTEROLS
- Publication
Frontiers in Immunology, 2024, p1
- ISSN
1664-3224
- Publication type
Article
- DOI
10.3389/fimmu.2024.1364161