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背景:G1期调节蛋白对调控增殖细胞的增殖周期具有重要作用,目前关于成骨细胞G1期调节蛋白的研究甚少,绝经后骨质疏松与成骨细胞G1期调节蛋白的关系更未被阐明。目的:观察去卵巢大鼠骨质疏松发病过程中成骨细胞G1期调节蛋白的改变,探讨绝经后骨质疏松症的发病机制。方法:100只6月龄SD雌性大鼠,随机分成假手术组和模型组各50只,模型组进行双侧卵巢结扎切除术,假手术组除未行卵巢结扎切除外,其余步骤与手术组相同。所有大鼠于术后4,8,12,18,24周分批取材,每批每组各处死10只,取大鼠腰椎。运用免疫组织化学方法检测骨组织中成骨细胞G1期调节蛋白CyclinD1、CDK4、p21蛋白表达。结果与结论:CyclinD1、CDK4蛋白阳性表达主要定位于骨小梁表面的成骨细胞。假手术组有CyclinD1、CDK4蛋白阳性表达,模型组表达强于假手术组。p21蛋白阳性表达部位与CyclinD1相似,假手术组和模型组均有明显阳性表达,但模型组的表达维持在较高水平,在各时期均明显高于同期假手术组(P<0.01)。结果证实,去卵巢骨质疏松模型大鼠发病过程中,成骨细胞CyclinD1、CDK4、p21蛋白出现明显高表达。提示成骨细胞增殖加快,同时成骨细胞周期受阻滞亦增多,成骨细胞数量相对不足,骨形成低于骨吸收,导致骨质疏松的发生。
BACKGROUND: G1 regulators play an important role in regulating the proliferative cycle of proliferating cells. At present, little is known about the regulation of G1 proteins in osteoblasts. The relationship between osteoporosis and osteoblast G1 regulators has not been elucidated yet . OBJECTIVE: To observe the changes of G1 phase regulatory proteins in osteoblasts during the pathogenesis of osteoporosis in ovariectomized rats and to explore the pathogenesis of postmenopausal osteoporosis. Methods: A total of 100 6-month-old SD female rats were randomly divided into sham operation group and model group, 50 in each group. The ovariectomized group was treated by bilateral ovariectomy. In the sham operation group, the same. All rats were drawn in batches at 4, 8, 12, 18 and 24 weeks after operation. 10 rats in each group were sacrificed and the lumbar vertebra was taken. Immunohistochemistry was used to detect the expression of CyclinD1, CDK4 and p21 proteins in osteoblasts. RESULTS AND CONCLUSION: The positive expression of CyclinD1 and CDK4 mainly localized on the surface of trabecular bone. The sham-operated group had positive expressions of CyclinD1 and CDK4 protein, while the expression in model group was stronger than that in sham-operated group. The positive expression site of p21 protein was similar to that of CyclinD1. The expression of p21 protein was significantly higher in sham operation group and model group than in sham operation group (P <0.01). The results confirmed that during the pathogenesis of ovariectomized osteoporosis model, the expression of CyclinD1, CDK4, p21 protein in osteoblasts was significantly high. Prompted the proliferation of osteoblasts accelerated, while osteoblast cell cycle arrest also increased, the relative lack of osteoblasts, bone formation below the bone resorption, leading to the occurrence of osteoporosis.