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姜黄素通过增加胆固醇外排发挥对巨噬细胞相关聚乙烯磨损颗粒诱导的炎症性骨溶解的保护作用。

Protection Effect of Curcumin for Macrophage-Involved Polyethylene Wear Particle-Induced Inflammatory Osteolysis by Increasing the Cholesterol Efflux.

机构信息

Department of Orthopaedics, Xiangya Hospital, Central South University, Changsha, Hunan, China (mainland).

出版信息

Med Sci Monit. 2019 Jan 1;25:10-20. doi: 10.12659/MSM.914197.

Abstract

BACKGROUND Periprosthetic osteolysis, induced by wear particles and inflammation, is a common reason for failure of primary arthroplasty. Curcumin, a nature phenol from plants, has been reported to reduce the inflammation in macrophages. This study aimed to investigate the potential effect of curcumin on macrophage involved, wear particle-induced osteolysis and its mechanism. MATERIAL AND METHODS RAW264.7 macrophages were used to test the effects of polyethylene (PE) particles and curcumin on macrophage cholesterol efflux and phenotypic changes. A mouse model of PE particle-induced calvarial osteolysis was established to test the effects of curcumin in vivo. After 14 days of treatment, the bone quality of the affected areas was analyzed by micro-computed tomography (micro-CT) and histology, and the bone surrounding soft tissues were analyzed at the cellular and molecular levels. RESULTS We found that PE particles can stimulate osteoclastogenesis and produce an M1-like phenotype in macrophages in vitro. Curcumin enhanced the cholesterol efflux in macrophages, and maintained the M0-like phenotype under the influence of PE particles in vitro. Additionally, the cholesterol transmembrane regulators ABCA1, ABCG1, and CAV1 were enhanced by curcumin in vivo. We also found enhanced bone density, reduced osteoclastogenesis, and fewer inflammatory responses in the curcumin treated groups in our mouse osteolysis model. CONCLUSIONS Our study findings indicated that curcumin can inhibit macrophage involved osteolysis and inflammation via promoting cholesterol efflux. Maintaining the cholesterol efflux might be a potential strategy to prevent periprosthetic osteolysis after total joint arthroplasty surgery.

摘要

背景

由磨损颗粒和炎症引起的假体周围骨溶解是初次关节置换失败的常见原因。姜黄素是一种来自植物的天然酚类化合物,已被报道可减少巨噬细胞中的炎症。本研究旨在探讨姜黄素对巨噬细胞参与、磨损颗粒诱导的骨溶解的潜在作用及其机制。

材料和方法

使用 RAW264.7 巨噬细胞来测试聚乙烯(PE)颗粒和姜黄素对巨噬细胞胆固醇流出和表型变化的影响。建立了 PE 颗粒诱导的颅骨骨溶解小鼠模型,以测试姜黄素在体内的作用。经过 14 天的治疗后,通过微计算机断层扫描(micro-CT)和组织学分析受影响区域的骨质量,并在细胞和分子水平上分析周围软组织中的骨。

结果

我们发现 PE 颗粒可以刺激破骨细胞形成,并在体外诱导巨噬细胞产生 M1 样表型。姜黄素增强了巨噬细胞中的胆固醇流出,并在 PE 颗粒的影响下维持了 M0 样表型。此外,姜黄素在体内增强了胆固醇跨膜调节剂 ABCA1、ABCG1 和 CAV1。我们还发现,在我们的小鼠骨溶解模型中,姜黄素治疗组的骨密度增加,破骨细胞形成减少,炎症反应减少。

结论

我们的研究结果表明,姜黄素可以通过促进胆固醇流出来抑制巨噬细胞参与的骨溶解和炎症。维持胆固醇流出可能是预防全关节置换术后假体周围骨溶解的一种潜在策略。

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