异补骨脂素调节JMJD3介导的H3K27me3去甲基化促进踝关节骨折大鼠骨重建
Isopsoralen promotes bone remodeling in ankle fracture rats by regulating H3K27me3 demethylation mediated by JMJD3
  
DOI:10.3969/j.issn.1006-7108.2026.05.010
中文关键词:  踝关节骨折  异补骨脂素  含Jumonji结构域3  H3K27三甲基化  骨重建
英文关键词:ankle fracture  isopsoralen  Jumonji domain containing 3  H3K27 trimethylation  bone remodeling
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段永富* 党兴 张铎安 韩雪来 南阳市第一人民医院骨二科,河南 南阳 473000 
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中文摘要:
      目的 探究异补骨脂素对踝关节骨折大鼠骨重建的影响及可能作用机制。方法 制备踝关节骨折大鼠模型,并进行异补骨脂素和GSK-J4治疗,大鼠分为对照组、模型组、异补骨脂素组、异补骨脂素+GSK-J4组。治疗8周后,观察大鼠踝关节骨折愈合和踝关节软骨损伤情况;检测踝关节Ⅱ型胶原(Collagen Ⅱ)、基质金属蛋白酶13(MMP-13)、含Jumonji结构域3(JMJD3)、H3K27三甲基化(H3K27me3)、Runt相关转录因子2(Runx2)和骨形态发生蛋白2(BMP2)表达水平。结果 异补骨脂素能够明显减轻大鼠关节间隙,改善软骨损伤,提高软骨组织JMJD3、Collagen Ⅱ、Runx2、BMP2表达,并降低Collagen Ⅱ、Runx2、BMP2启动子H3K27me3水平及H3K27me3蛋白表达(P<0.05);GSK-J4能够抑制异补骨脂素对大鼠骨重建的改善作用(P<0.05)。结论 异补骨脂素通过增强JMJD3介导的H3K27me3去甲基化,促进踝关节骨折大鼠骨重建。
英文摘要:
      Objective To explore the effect and possible mechanism of Isopsoralen on bone remodeling in ankle fracture rats. Methods Rat model of ankle joint fracture was prepared and treated with isopsoralen and GSK-J4, Rats were divided into Control group, Model group, Isopsoralen group and Isopsoralen+GSK-J4 group. After 8 weeks of treatment, The healing of ankle fractures and ankle cartilage injuries in rats were observed; The expression of Collagen Ⅱ, matrix metalloproteinase 13 (MMP-13), Jumonji domain containing 3 (JMJD3), H3K27 trimethylation (H3K27me3), Runt related transcription factor 2 (Runx2) and bone morphogenetic protein 2 (BMP2) levels in ankle joint were detected. Results Isopsoralen could significantly reduce the joint space in rats, improved cartilage damage, increased the expression of JMJD3, Collagen Ⅱ, Runx2, BMP2 in cartilage tissue, and reduced the levels of Collagen Ⅱ, Runx2, BMP2 promoter H3K27me3 and the expression of H3K27me3 protein (P<0.05); GSK-J4 could inhibit the improvement effect of Isopsoralen on bone remodeling in rats (P<0.05). Conclusion Isopsoralen promotes bone remodeling in ankle fracture rats by enhancing JMJD3 mediated H3K27me3 demethylation.
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