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作 者:童培建[1] 肖鲁伟[2] 季卫锋[1] 田琨[1]
机构地区:[1]浙江中医药大学附属第一医院骨伤科,浙江杭州310006 [2]浙江中医药大学
出 处:《中国骨伤》2009年第2期110-113,共4页China Journal of Orthopaedics and Traumatology
基 金:浙江省自然科学基金资助项目(编号:Z303656)
摘 要:目的:通过诱导激素性股骨头坏死的动物模型并观测模型的相关指标,研究脂质代谢及破骨细胞活性在激素性股骨头坏死塌陷发生过程中的作用。方法:将雄性SD大鼠40只(150g左右),随机分为空白对照组和激素实验组,腹腔注射大肠杆菌内毒素后,实验组每周1次臀肌注射醋酸强的松龙35.5mg/kg,对照组每周1次臀肌注射生理盐水2ml,于第12周用药结束后处死动物,进行血清抗酒石酸酸性磷酸酶5b(Trap-5b)、总胆固醇(TC)、甘油三酯(TG)、软骨下骨生物力学、股骨骨密度测定,制作HE染色病理切片,进行茜红素和抗酒石酸酸性磷酸酶(TRACP)染色,并进行统计分析。结果:实验组的血清总胆固醇、甘油三酯、抗酒石酸酸性磷酸酶5b含量显著升高(P<0.01),局部骨髓内出现大量破骨细胞,骨质丢失严重(P<0.01),软骨下骨生物力学性能显著下降(P<0.01)。结论:脂质代谢紊乱是激素性股骨头坏死重要的发病机制;破骨细胞活性增强、数量增加,引起骨质严重丢失导致的软骨下骨生物力学性能下降是股骨头塌陷的直接原因。Objective : To explore the role of metabolism of fatty substance and osteoclast activity during the process of steroid-induced necrosis of femoral head through mice model inducing and model index measurement. Methods: Forty SD male mice were divided into 2 groups randomly, the control group and the experiment group. After the gluteal injection of colibacillus endotoxin,the experiment group was given gluteal injection of prednisolone acetate 35.5 mg/kg per week,and 2 ml of normal saline to the control group. The mice were killed 12 weeks later and tested the content of Trap-Sb,TC and TG of the blood serum. Vitodynamies, bone density were measured and sections of HE staining, Ca^2+ and TRACP staining was made then statistic analysis was performanced. Results :The content of TC ,TG and Trap-5b increased apparently (P〈0.01). Large amount of osteoclasts were found in local medullary cavity. There was severe bone loss and decrease of vitodynamics in subchondral bone (P〈0.01)in experiment group. Conclusion:Metabolic disorder of fatty substance is the key pathogenesis of steroid-induced avascular necrosis of femoral head. Decrease of vitodynamics in subchondral bone due to hyperactivity and increase of osteo- clast lead to collapse of femoral head directly.
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