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目的:比较1,25(OH)2D3缺失对膜内成骨和软骨内成骨影响的不同。方法:用免疫组织化学染色、HE染色和Western-blot等方法检测6周龄的野生型(wild type,WT)和1琢(OH)ase-/-小鼠的颅骨和股骨干骺端骨组织中I型胶原和甲状旁腺素受体(parathyroid hormone receptor,PTHR)的表达水平。结果:和WT小鼠相比较,1 ase-/-小鼠颅骨的I型胶原阳性面积明显减少,但是干骺端I型胶原阳性面积明显增加,差异有显著性(P<0.01);1琢(OH)ase-/-小鼠颅骨成骨细胞计数明显减少,差异存在统计学意义(P<0.05);但是干骺端成骨细胞计数明显增加,差异有显著性(P<0.01);1琢(OH)ase-/-小鼠颅骨的PHTR表达水平明显减少,但是在干骺端PHTR表达水平明显增加,差异均有显著性(P<0.01)。结论:1,25(OH)2D3缺乏导致小鼠膜内成骨方式骨形成减少,而软骨内成骨骨形成增加。
OBJECTIVE: To compare the effects of 1,25 (OH) 2D3 deficiency on intraosseous and intrachondral bone formation. Methods: The skull and femoral metaphyseal bone tissue of 6-week-old wild-type (WT) and 1-cut (OH) ase - / - mice were detected by immunohistochemical staining, HE staining and Western- In type I collagen and parathyroid hormone receptor (parathyroid hormone receptor, PTHR) expression levels. Results: Compared with WT mice, the positive area of type I collagen in the skull of 1 ase - / - mice was significantly decreased, but the positive area of type I collagen in metaphyseal tissues was significantly increased (P <0.01) (OH) ase - / - mice, the difference was statistically significant (P <0.05); however, the counts of metaphyseal osteoblasts were significantly increased (P <0.01); 1 The expression of PHTR in skull of mice with OH (OH) ase - / - mice obviously decreased, but the PHTR expression in metaphysis was significantly increased (P <0.01). CONCLUSION: Lack of 1,25 (OH) 2D3 results in reduced osteogenesis in mouse membrane and increased osteochondral bone formation in mice.