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| 云克治疗糖皮质激素性骨质疏松模型大鼠的实验研究 |
| Experimental study of 99Tc-MDP on the treatment of glucocorticoid-induced osteoporosis in rats |
| 投稿时间：2012-10-27 |
| DOI： |
| 中文关键词: 锝亚甲基二磷酸盐 糖皮质激素性骨质疏松 骨保护素 |
| 英文关键词:99Tc-MDP Glucocorticoid-induced osteoporosis Osteoprotegerin |
| 基金项目:内蒙古自治区卫生科研基金项目：锝亚甲基二膦酸盐对去卵巢大鼠OPG/RANKL/RANK系统和骨结构的影响（2010160） |
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| 中文摘要: |
| 目的 探讨云克对地塞米松诱导的骨质疏松症大鼠的治疗作用.方法 12周龄的雌性Wistar大鼠30只,随机分为3组,对照组、模型组和治疗组,每组10只.模型组和治疗组给予5mg/kg地塞米松肌注,1次/周,连续注射12周,对照组肌注等剂量的生理盐水.DEXA骨密度仪检测大鼠股骨骨密度,各组均取2只处死,HE染色观察股骨结构的病理改变鉴定骨质疏松大鼠模型是否构建成功.骨质疏松模型构建成功后,治疗组大鼠尾静脉注射云克(0.05 μg/kg),对照组和模型组注射等剂量的生理盐水,1次/周,连续注射15周,治疗前后尾静脉采血,ELISA法检测血清骨碱性磷酸酶和酒石酸酸性磷酸酶水平的变化.检测各组大鼠治疗后的股骨骨密度,之后,处死各组大鼠,取股骨,免疫组化法检测大鼠股骨骨保护素的变化,HE染色观察骨结构的病理改变.结果 (1)模型组和治疗组大鼠经地塞米松处理12周后,股骨骨密度较对照组明显降低(P＜0.05)；病理改变为骨小梁稀疏、数目明显减少甚至断裂,而对照组骨小梁结构较完整.(2)与模型组相比,治疗组大鼠血清骨特异碱性磷酸酶水平明显升高(P＜0.05),而抗酒石酸酸性磷酸酶水平有所下降,但无统计学差异(P＞0.05).(3)治疗组治疗后血清骨特异碱性磷酸酶水平明显升高(P＜0.05),而抗酒石酸酸性磷酸酶水平有所下降,但无统计学差异(P＞0.05).(4)与模型组和治疗前相比,治疗组大鼠股骨骨密度无明显改变(P＞0.05).(5)与模型组相比,治疗组大鼠股骨骨保护素表达明显增加.(6)云克治疗后,治疗组大鼠股骨有新生骨小梁的广泛形成,骨小梁结构破坏较模型组明显减轻.结论 云克对糖皮质激素性骨质疏松大鼠有治疗作用. |
| 英文摘要: |
| Objective To explore the therapeutic efficacy of 99Tc-MDP on rats with dexamethasone-induced osteoporosis. Methods Thirty 12-week female Wistar rats were randomly divided into three groups: control group, model group, and treatment group. Each group had 10 rats. Rats in model group and treatment group received an intramuscular injection of 5mg/kg dexamethasone once a week for 12 weeks continuously. Rats in control group received an injection of the same dose of normal saline. Bone mineral density of the femur was detected using DEXA. Two rats from each group were killed. The pathological changes of the femoral structure were observed after HE staining, in order to identify the successful establishment of osteoporosis model. After the successful establishment of osteoporosis model, rats in treatment group received an injection of 0.05μg/kg MDP through tail vein. Meanwhile, rats in control group and model group received an injection of the same dose of normal saline once a week for 15 weeks continuously. Venous blood from tail vein before and after the treatment was collected. Changes of serum levels of alkaline phosphatase and tartrate acid phosphatase were detected using ELISA. Bone mineral density of the femur in each group was detected. Then all of rats were sacrificed, and the femurs were collected. At last, the changes of osteoprotegerin (OPG) in the femur were detected using immunohistochemical staining. Pathological changes of bone structure were observed after HE staining. Results Comparing with that in control group, bone mineral density of the femur in model group and treatment group decreased significantly after 12-week treatment of dexamethasone (P<0.05). Pathological changes included sparse trabecular, reduced trabecular number, and even broken trabecular, while trabecular observed in control group was relatively integrated. Comparing with that in model group, serum levels of bone-specific alkaline phosphatase (BALP) increased significantly in treatment group (P<0.05), while serum level of tartrate-resistant acid phosphatase (TARP) declined, but no significant difference was observed (P>0.05). Serum level of BALP after the treatment in treatment group was significantly higher than that before the treatment (P<0.05), while serum level of TARP declined, but no significant difference was observed (P>0.05). Bone mineral density of the femur after the treatment in treatment group had no significant difference comparing with that in model group or that before the treatment (P>0.05). Comparing with that in model group, the expression of OPG in the femur increased significantly in treatment group. Comparing with that in model group, extensive formation of new trabecular and less trabecular damage was observed in treatment group after MDP treatment. Conclusion MDP is effective in the treatment of glucocorticoid-induced osteoporosis in rats. |
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