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冬凌草甲素抑制破骨细胞分化的机制研究
雷新环1, 李芷嫣, 黄微星, 蔡国平, 米爽, 洪盾, 章礼炜
浙江省台州医院骨外科
摘要:
目的探讨冬凌草甲素抑制破骨细胞分化的作用及其机制。方法通过体外培养原代骨髓巨噬细胞(BMMs),观察不同浓度冬凌草甲素对BMMs增殖的抑制作用和破骨细胞分化的影响;抗酒石酸酸性磷酸酶(TRAP)染色观察破骨细胞数目和铺展率;qRT-PCR法检测破骨细胞降钙素受体(CTR)、组织蛋白酶K(CTSK)、活性T细胞核因子c1(NFATc1)mRNA表达水平。结果与对照组相比,经冬凌草甲素处理48、72h后,6.4滋M以上的冬凌草甲素对BMMs的增殖有明显抑制作用,差异均有统计学意义(均P<0.05);经冬凌草甲素处理96h后,3.2滋M以上的冬凌草甲素对BMMs的增殖有明显抑制作用,差异均有统计学意义(均P<0.01);在NF-资B受体活化因子配体诱导下,与对照组相比,0.4、0.8滋M冬凌草甲素可明显减少破骨细胞分化数目和铺展率(均P<0.01),且其CTR、CTSK、NFATc1mRNA表达水平均下调(均P<0.01)。结论冬凌草甲素通过下调破骨细胞分化转录调控因子NFATc1的表达抑制破骨细胞的分化。
关键词:  冬凌草甲素 破骨细胞 细胞分化
DOI:10.12056/j.issn.1006-2785.2018.40.12.2018-403
分类号:
基金项目:
Effect of Oridonin on proliferation and differentiation of osteoclasts and its mechanisms
Abstract:
Objective To investigate the effect of oridonin on proliferation and differentiation of osteoclasts and its mechanism. Methods The mouse primary bone marrow-derived macrophages(BMMs) were isolated and treated with 50ng/ml RANKL and 30ng/ml M-CSF to differentiate to osteoclasts. BMMs were treated with different concentration of oridonin and the cell proliferation was determined by CCK-8 assay. Under RANKL stimulation, the number and area of osteoclast were measured by anti-tartaric acid staining(TRAP); the expression of osteoclast-related genes was detected by qRT-PCR. Results Compared to the control group, after treated by>6.4滋M oridonin for 48 and 72h, or by>3.2滋M toridonin for 96h the proliferation of BMMs was significantly inhibited (all P<0.05 ). Compared to the control group, after treated with 0.4 and 0.8滋M oridonin for 96h, the number and area of osteoclast were significantly reduced( all P< 0 . 01 ) , the expressions of CTR , CTSK and NFATc1 mRNA were suppressed (all P<0.01). Conclusion Oridonin inhibits osteoclast differentiation via suppressing NFATc1 expression.
Key words:  Oridonin Osteoclasts Cell Differentiation