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目的从体外和体内实验2个方面评价柚皮苷对聚甲基丙烯酸甲酯(PMMA)诱发的破骨细胞性骨溶解的作用。方法培养破骨细胞前体细胞RAW264.7,使用PMMA颗粒刺激细胞,观察柚皮苷的治疗作用。检测抗酒石酸酸性磷酸酶(TRAP)染色、Ca2+释放实验以及TRAP、组织蛋白酶(CPK)、NF-κB的基因表达。采用小鼠膝关节置钉模型评价柚皮苷对PMMA诱发骨吸收的作用,对实验标本采用生物力学拔出试验进行评价。结果柚皮苷可以有效地抑制破骨细胞的形成并下调骨吸收基因标记物的表达,剂量为10μg/ml时表现出对TRAP活性的最大抑制作用。在颗粒刺激培养液中柚皮苷降低了钙的释放。柚皮苷缓解了膝关节置钉模型中PMMA颗粒刺激所造成的长期的骨吸收,表现为骨体积分数的增加和最大钉拔出力的增加。300 mg/kg的灌胃剂量可达到最好的疗效。结论柚皮苷抑制PMMA诱导的破骨细胞形成,降低PMMA颗粒刺激的钙释放。在观察慢性骨吸收的长期模型中,柚皮苷也有效抑制PMMA诱发的骨吸收,并保留了置入物的稳定性。
Objective To evaluate the effect of naringin on polymethylmethacrylate (PMMA) -induced osteoclastic osteolysis in vitro and in vivo. Methods Cultured osteoclast precursor cells RAW264.7, the use of PMMA particles to stimulate cells to observe the therapeutic effect of naringin. The tartrate-resistant acid phosphatase (TRAP) staining, Ca2 + release assay and gene expression of TRAP, cathepsin (CPK) and NF-κB were detected. The effect of naringin on bone resorption induced by PMMA was evaluated by the mouse knee arthroplasty model. The biomechanical pull-out test was used to evaluate the experimental specimens. Results Naringin effectively inhibited the formation of osteoclasts and down-regulated the expression of bone resorption markers. The maximum inhibitory effect on TRAP activity was observed at 10 μg / ml. Naringin reduced the release of calcium in the granule stimulated culture. Naringin relieved long-term bone resorption caused by PMMA particle stimulation in the knee arthroplasty model, as demonstrated by an increase in bone volume fraction and an increase in maximal nail pull-out force. 300 mg / kg gavage dose to achieve the best effect. Conclusion Naringin inhibits PMMA-induced osteoclast formation and decreases PMMA-stimulated calcium release. In the long-term model of chronic bone resorption, naringin also effectively inhibits PMMA-induced bone resorption and preserves the stability of the implant.