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目的:通过检测孕期尼古丁暴露胎鼠长骨病理学变化和尼古丁处理后原代成骨细胞基因表达的影响,探讨尼古丁影响长骨发育的可能机制。方法:健康Wistar雌性大鼠受孕后第9天起皮下注射给予尼古丁2 mg/(kg·d),孕20d处死孕鼠收集胎骨,检测骨化中心病理学变化和基因表达;在原代成骨细胞成骨分化模型上给予不同浓度尼古丁处理7d,检测成骨和破骨分化基因表达。结果:与对照组相比,尼古丁组胎鼠股骨缩短,初级骨化中心长度缩短;尼古丁处理下调成骨细胞成骨分化基因runt相关转录因子2(Runx2)、骨钙素(BGLAP)和骨涎蛋白(BSP)的表达,抑制破骨细胞分化因子(RANKL)表达,并呈现良好的剂量依赖关系。结论:孕期尼古丁暴露子代大鼠存在长骨发育迟缓,可能与成骨分化功能抑制有关。
OBJECTIVE: To explore the possible mechanism of nicotine influencing the development of long bones by examining the effects of nicotine on the long bone pathology and nicotine-treated primary osteoblasts during pregnancy. METHODS: Healthy Wistar female rats were injected nicotine 2 mg / (kg · d) subcutaneously on the 9th day after conception. The fetuses were collected from pregnant rats on the 20th day of gestation. The pathological changes and gene expression of ossification center were detected. Nicotine of different concentrations was treated for 7 days on osteoblast differentiation model to detect osteogenic and osteoclastic gene expression. Results: Compared with the control group, the nicotine of the nicotine group was shortened and the length of the primary ossification center was shortened. Nicotine decreased the expression of osteoblast differentiation gene Runx2, osteocalcin (BGLAP) Protein (BSP) expression, inhibition of osteoclast differentiation factor (RANKL) expression, and showed a good dose-dependent relationship. Conclusion: Nicotine exposure progeny during pregnancy has long bone growth retardation, which may be related to the inhibition of osteogenic differentiation.