Rutin Inhibits Ox-LDL-Mediated Macrophage Inflammation and Foam Cell Formation by Inducing Autophagy and Modulating PI3K/ATK Signaling |
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Authors: | Ben Li Yumeng Ji Chenlong Yi Xufeng Wang Chaoyang Liu Chufan Wang Xiaohu Lu Xiaohan Xu Xiaowei Wang |
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Affiliation: | 1.Department of Cardiovascular Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210000, China; (B.L.); (Y.J.); (X.W.); (C.L.); (C.W.); (X.L.);2.The First Clinical School of Medicine, Nanjing Medical University, Nanjing 210000, China;3.Department of Cardiovascular Surgery, Yangzhou First People’s Hospital, Yangzhou 225000, China; |
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Abstract: | Atherosclerosis (AS) is one of the leading causes of death among the elderly, and is primarily caused by foam cell generation and macrophage inflammation. Rutin is an anti-inflammatory, anti-oxidant, anti-allergic, and antiviral flavonoid molecule, known to have anti-atherosclerotic and autophagy-inducing properties, but its biological mechanism remains poorly understood. In this study, we uncovered that rutin could suppress the generation of inflammatory factors and reactive oxygen species (ROS) in ox-LDL-induced M2 macrophages and enhance their polarization. Moreover, rutin could decrease foam cell production, as shown by oil red O staining. In addition, rutin could increase the number of autophagosomes and the LC3II/I ratio, while lowering p62 expression. Furthermore, rutin could significantly inhibit the PI3K/ATK signaling pathway. In summary, rutin inhibits ox-LDL-mediated macrophage inflammation and foam cell formation by inducing autophagy and modulating PI3K/ATK signaling, showing potential in treating atherosclerosis. |
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Keywords: | rutin atherosclerosis RAW264.7 inflammation autophagy |
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