文章摘要
李志伟,任然悦,李孟伟,等.淫羊藿苷通过促进负调控因子Gα13的表达抑制破骨细胞形成.骨科,2022,13(2): 155-159.
淫羊藿苷通过促进负调控因子Gα13的表达抑制破骨细胞形成
Icariin Inhibits Osteoclast Formation by Promoting the Expression of Negative Regulator Gα13
投稿时间:2021-10-19  
DOI:10.3969/j.issn.1674-8573.2022.02.012
中文关键词: 淫羊藿苷  破骨细胞  骨质疏松  鸟嘌呤核苷酸结合蛋白亚基α13
英文关键词: Icariin  Osteoclastogenesis  Osteoporosis  Gα13
基金项目:
作者单位E-mail
李志伟 华中科技大学同济医学院附属同济医院骨科武汉430030  
任然悦 华中科技大学同济医学院附属同济医院骨科武汉430030  
李孟伟 华中科技大学同济医学院附属同济医院骨科武汉430030  
刘起昆 华中科技大学同济医学院附属同济医院骨科武汉430030  
于小钧 华中科技大学同济医学院附属同济医院骨科武汉430030  
蒋咏桥 华中科技大学同济医学院附属同济医院骨科武汉430030  
鲍远 华中科技大学同济医学院附属同济医院骨科武汉430030  
康皓 华中科技大学同济医学院附属同济医院骨科武汉430030 kanghao100@vip.sina.com 
摘要点击次数: 2389
全文下载次数: 2573
中文摘要:
      目的 研究淫羊藿苷对破骨细胞分化和鸟嘌呤核苷酸结合蛋白亚基α13(Gα13)介导的信号通路的影响,探讨淫羊藿苷治疗骨质疏松的可能机制。方法 从C57/BL6小鼠四肢骨骨髓中提取原代单核巨噬细胞(bone marrow derived macrophages,BMMs),使用核因子κB受体活化因子配体(receptor activator of nuclear factor-κB ligand,RANKL)和巨噬细胞集落刺激因子(macrophage colony-stlimulating factor,M-CSF)将BMMs诱导成破骨细胞。同时使用不同浓度(0、1、10 μmol/L)的淫羊藿苷进行干预,采用抗酒石酸酸性磷酸酶(TRAP)和鬼笔环肽染色、qPCR和Western blot等实验分析淫羊藿苷对破骨细胞形成及其对Gα13基因和Akt-GSK3β-NFATc1信号通路相关基因表达的影响。结果 TRAP染色和鬼笔环肽染色结果显示淫羊藿苷可显著抑制破骨细胞形成(P<0.05)。淫羊藿苷显著促进Gα13基因及蛋白表达(P<0.05),显著抑制Akt-GSK3β-NFATc1信号通路相关基因及蛋白的表达(P<0.05)。结论 淫羊藿苷可能是通过促进负调控因子Gα13的表达,从而抑制其下游Akt-GSK3β-NFATc1信号通路来抑制破骨细胞形成。
英文摘要:
      Objective To investigate the effects of icariin on osteoclastogenesis and to elucidate the mechanism of guanine nucleotide-binding protein subunit α13 (Gα13) underlying this effect, and the possible mechanism of icariin in the treatment of osteoporosis. Methods Bone marrow derived macrophages (BMMs) were extracted from the bone marrow of the femurs and tibias of C57/BL6 mice, and the BMMs were induced into osteoclasts by receptor activator of nuclear kappa B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). At the same time, BMMs were treated with different icariin concentrations (0, 1, 10 μmol/L). TRAP and F-actin ring staining, qPCR and Western blotting were performed in this study. Results TRAP staining and Actin ring formation assays showed that icariin inhibited RANKL-induced osteoclast formation (P<0.05). Icariin could significantly promote the expression of Gα13 gene and its related proteins (P<0.05), and significantly inhibit the expression of Akt, NFATc1 related genes and proteins. Conclusion Icariin significantly up-regulates the expression of negative regulator Gα13 and activates Gα13 to inhibit osteoclast formation through the Akt-GSK3β-NFATC1 signaling pathway.
查看全文   下载PDF阅读器
关闭