加速高密度脂蛋白介导的胆固醇外流可缓解牙周炎。

Journal of dental research Pub Date : 2024-10-01 Epub Date: 2024-09-23 DOI:10.1177/00220345241271075
T-T Tran, G Lee, Y H Huh, K-H Chung, S Y Lee, K H Park, J-H Kim, M-S Kook, J Ryu, O-S Kim, H-P Lim, J-T Koh, J-H Ryu
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引用次数: 0

摘要

牙周炎(PD)是一种常见的炎症性疾病,已知与代谢紊乱,尤其是高脂血症密切相关。在本研究中,我们证实高胆固醇血症是牙周炎发病的一个易感因素。逻辑回归分析表明,帕金森病与血脂异常之间存在很强的正相关性。体内(高胆固醇饮食下的 PD 小鼠模型)和体外(胆固醇处理牙龈成纤维细胞 [GFs])实验的数据显示,过量胆固醇流入牙龈成纤维细胞可能会导致牙周炎症,进而造成牙槽骨侵蚀。此外,我们还比较了不同作用模式的降胆固醇药物对小鼠肺结核发病机制的保护作用。在我们测试的降胆固醇药物中,非诺贝特对帕金森病发病机制的保护作用最强,因为它能提高高密度脂蛋白胆固醇的水平,而高密度脂蛋白胆固醇参与细胞中胆固醇的外流和胆固醇的逆向转运。事实上,在帕金森氏症进展过程中,胆固醇外流会因载脂蛋白A-I结合蛋白(APOA1BP)在发炎的GFs中表达下调而受到抑制。我们还证明,过量表达 APOA1BP 可通过诱导胆固醇外流有效调节牙周炎症和随后的牙槽骨流失。我们的研究结果凸显了目前可用的降胆固醇药物在缓解牙周病发病机制方面的潜在作用。通过以加速高密度脂蛋白介导的细胞胆固醇外流为目标,一种新的治疗脑退化症的方法可能成为可能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Acceleration of HDL-Mediated Cholesterol Efflux Alleviates Periodontitis.

Periodontitis (PD) is a common inflammatory disease known to be closely associated with metabolic disorders, particularly hyperlipidemia. In the current study, we demonstrated that hypercholesterolemia is a predisposing factor in the development of PD. Logistic regression analysis revealed a strong positive correlation between PD and dyslipidemia. Data from in vivo (PD mouse model subjected to a high cholesterol diet) and in vitro (cholesterol treatment of gingival fibroblasts [GFs]) experiments showed that excess cholesterol influx into GFs potentially contributes to periodontal inflammation and, subsequently, alveolar bone erosion. Additionally, we compared the protective efficacies of cholesterol-lowering drugs with their different modes of action against PD pathogenesis in mice. Among the cholesterol-lowering drugs we tested, fenofibrate exerted the most protective effect against PD pathogenesis due to an increased level of high-density lipoprotein cholesterol, a lipoprotein involved in cholesterol efflux from cells and reverse cholesterol transport. Indeed, cholesterol efflux was suppressed during PD progression by downregulation of the apoA-I binding protein (APOA1BP) expression in inflamed GFs. We also demonstrated that the overexpression of APOA1BP efficiently regulated periodontal inflammation and the subsequent alveolar bone loss by inducing cholesterol efflux. Our collective findings highlight the potential utility of currently available cholesterol-lowering medications for the mitigation of PD pathogenesis. By targeting the acceleration of high-density lipoprotein-mediated cellular cholesterol efflux, a new therapeutic approach for PD may become possible.

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