12-Deoxyphorbol 13-acetate 通过减弱 MAPK 信号传导和 NFATc1 激活来抑制 RANKL 诱导的破骨细胞生成。,International Immunopharmacology

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12-Deoxyphorbol 13-acetate 通过减弱 MAPK 信号传导和 NFATc1 激活来抑制 RANKL 诱导的破骨细胞生成。
International Immunopharmacology ( IF 4.8 ) Pub Date : 2021-10-07 , DOI: 10.1016/j.intimp.2021.108177
Delong Chen ₁ , Feifan Chu ₂ , Gangyu Zhang ₃ , Qingqing Wang ₄ , Ying Li ₅ , Meng Zhang ₆ , Qi He ₃ , Junzheng Yang ₃ , Haibin Wang ₇ , Ping Sun ₈ , Jiake Xu ₉ , Peng Chen ₇

Affiliation

Department of Orthopaedic Surgery, Clifford Hospital, Jinan University, Guangzhou 510006, China.
The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, China.
Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
Department of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou 310000, China.
Department of Orthopaedic Surgery, The Third Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou 510360, China.
Department of Orthopedics, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, People's Hospital of Henan University, Zhengzhou 450003, China.
Department of Orthopaedic Surgery, The First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
Department of Endocrinology, The First Affiliated Hospital, Guangdong Pharmaceutical University, Guangzhou 510000, China.
School of Biomedical Sciences, University of Western Australia, Perth, Western Australia 6009, Australia.

当破骨细胞活性超过成骨细胞活性时，就会发生骨质疏松症，其特征是骨质流失和微结构损伤。已证明对破骨细胞分化和功能具有抑制作用的天然化合物可预防骨质疏松症。经过多种化合物筛选后，发现 12-脱氧佛波醇 13-乙酸酯 (DPA) 通过减弱 NFATc1 和 c-Fos 的活性以剂量依赖性方式降低 RANKL 诱导的破骨细胞生成，然后降低破骨细胞功能相关基因和蛋白质（包括 Acp5）的水平、V-ATPase-d2 和 CTSK。机制上，我们发现 DPA 抑制 RANKL 诱导的下游信号通路，包括 MAPK 信号通路和钙振荡。此外，在 OVX 诱导的骨质疏松小鼠模型中进一步证实了 DPA 的体内功效。集体，

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更新日期：2021-10-06

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