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银杏双黄酮抑制NF-κB信号通路影响骨髓巨噬细胞向破骨细胞分化

吴 锋, 曾 艳平, 覃 万安, 林 舟丹, 程 昌志, 梁 雄波, 陈 子阳, 韦 葛堇
中国人民解放军联勤保障部队第九二三医院

摘要


目的本研究基于NF-κB通路探讨银杏双黄酮(ginkgetin,GK)对RANKL诱导的破骨细胞分化的影响及其作用机制。方法采用不同浓度的GK(0、0.1、1、10和100µM)作用小鼠骨髓来源的巨噬细胞(BMMs)并分组,通过CCK8试剂检测各组的细胞增殖,TRAP染色检测破骨细胞生成能力,通过Western-blot检测IκBα蛋白表达。结果高浓度GK(大于12.5µM)可显著抑制BMMs增殖,TRAP染色显示高浓度GK抑制破骨细胞形成,Western-blot结果显示,GK(50µM)组IκBα表达明显高于对照组。结论在小鼠BMMs中,GK可抑制NF-κB信号通路进而影响RANKL诱导的破骨细胞分化。

关键词


银杏双黄酮,NF-κB。骨质疏松症,破骨细胞,RANKL

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参考


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DOI: http://dx.doi.org/10.12361/2705-0459-05-03-125347

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