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作 者:付福建 郑周海 史晓红 娄方练 宋飞 刘睿 Fu Fujian;Zheng Zhouhai;Shi Xiaohong;Lou Fanglian;Song Fei;Liu Rui(The People's Hospital of Nanchuan,Chongqing,408400)
机构地区:[1]重庆市南川区人民医院
出 处:《基因组学与应用生物学》2019年第10期4726-4731,共6页Genomics and Applied Biology
摘 要:尽管近年来骨质流失的相关机制研究越来越多,但双膦酸盐治疗骨质疏松性髋骨部骨折的作用机理仍还未被充分认识。为了探讨双磷酸盐对破骨细胞的作用机理,本研究借助流式细胞仪检测了破骨细胞的凋亡坏死情况;通过免疫荧光实验表征了破骨细胞肌动蛋白,以及重要的雌激素受体α(ERα)蛋白因子变化情况。结果表明:阿仑膦酸钠强烈诱导了破骨细胞凋亡,同时介导肌动蛋白不规则化,引发细胞结构坍塌;阿仑膦酸钠以增强ERα活性的方式,协同诱导了细胞凋亡,抑制破骨细胞分化成熟。阿仑膦酸钠通过作用于ERα和肌动蛋白因子,负面调节破骨细胞的形成和功能,介导破骨细胞凋亡,限制细胞寿命,防止中老年人过多的骨质流失,从而促进骨重建平衡。Although the mechanism of bone loss has been increasing in recent years,the mechanism of bisphosphonates in the treatment of osteoporotic hip fractures is still not fully understood.In combination with apoptosis research methods,the mechanism of bisphosphonate on osteoclasts was investigated.Apoptosis of osteoclasts was detected by flow cytometry.The changes of osteoclast actin and important estrogen receptor alpha(ERα)protein factors were characterized by immunofluorescence experiments.Alendronate strongly induced osteoclast apoptosis and mediates cell structure collapse caused by actin irregularities.In addition,synergistic induction of apoptosis and inhibition of osteoclasts differentiation in a manner that enhances ERαactivity.Alendronate inhibits the formation and function of osteoclasts by acting on ERαand actin factors,mediates osteoclast apoptosis,limits cell life and prevents excessive bone loss in middle-aged and elderly people.
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