Modulation of lectin-like oxidized low-density lipoprotein receptor-1 by Porphyromonas gingivalis promoting progression of atherosclerosis in apolipoprotein E(-/-) mice

牙龈卟啉单胞菌通过调节凝集素样氧化低密度脂蛋白受体-1促进载脂蛋白E(-/-)小鼠动脉粥样硬化的进展

阅读:2

Abstract

BACKGROUND/PURPOSE: Porphyromonas gingivalis (P. gingivalis), the primary pathogenic bacterium in periodontitis, can infiltrate the cardiovascular system via the bloodstream and actively contribute to various pathological processes associated with atherosclerosis. The scavenger receptor lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) plays a crucial role in atherosclerosis pathogenesis. Previous studies have shown that LOX-1 is involved in endothelial cell activation injury, monocyte migration, and adhesion to endothelial cells induced by P. gingivalis. The objective of this study was to further investigate the potential role of LOX-1 in promoting P. gingivalis-induced atherosclerosis in mice. MATERIALS AND METHODS: Using apolipoprotein E (APOE)(-/-) mice fed with high-fat diet for an established model. Intravenous injection of P. gingivalis was performed to create P. gingivalis blood model while intraperitoneal injection of Polyinosinic-polycytidylic acid (Poly (I:C)) served as an inhibitor for LOX-1. After 12 weeks, plaques and blood lipids were examined. RESULTS: Results showed that induction with P. gingivalis led to increased expression of LOX-1 in both the aortic root and blood samples, increased plaque area, reduced plaque stability, elevated expression levels of vascular adhesion molecule-1(VCAM-1), Interleukin-6(IL-6) and M1 macrophages. However, pretreatment with Poly (I:C) resulted in decreased plaque area improved plaque stability and reduced expression levels of VCAM-1 and IL-6. CONCLUSION: These findings suggest that LOX-1 may serve as an intermediary factor promoting atherosclerosis associated with periodontitis.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。