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作 者:吴鹰[1] 何波[2] 刘淑娟[2] 闫鸿丽[2] 云宇[3] 沈志强[2]
机构地区:[1]云南大理学院内科教研室,大理671003 [2]昆明医学院云南省天然药物药理重点实验室 [3]昆明医学院药理教研室,昆明650031
出 处:《昆明医学院学报》2006年第6期9-15,T0002,共8页Journal of Kunming Medical College
基 金:国家自然科学基金资助(30660212);云南省自然科学基金资助(2004C0044M)
摘 要:目的评价老鹳草素(geraniin,Ge)对实验性骨质疏松症的影响并探讨其初步作用机制.方法用维甲酸建立大鼠骨质疏松模型,观察Ge 20 mg/kg灌胃给药1周后对骨质疏松相关指标的影响.机械法分离1日龄SD大鼠四肢长骨获得破骨细胞(osteoclast,OC),接种于培养板中培养,在培养液中分别加入不同浓度的Ge和Ⅱ型碳酸酐酶(carbonic anhydraseⅡ,CAⅡ)阻断剂乙酰唑胺(acetazolamide,Az),应用抗酒石酸酸性磷酸酶(tartrate-resistant acid phosphatase,TRAP)和甲苯胺蓝染色技术,观察不同浓度Ge对OC生存率的影响.结果维甲酸70 mg/kg体重灌胃15 d,模型组大鼠的体重下降,卵巢指数下降,血清碱性磷酸酶(alkaline phosphatase,ALP)升高,骨钙含量减少,骨小梁稀疏,骨小梁表面积减小,骨小梁间隙面积增大,表明大鼠骨质疏松模型复制成功.与模型组比较,Ge组和尼尔雌醇片阳性对照组的卵巢指数高,骨钙增高,骨小梁较密集,骨小梁间隙面积小,骨小梁表面积大,Ge可降低血清ALP同时升高血清钙水平.Ge呈浓度依赖性减少体外培养的TRAP染色阳性的多核细胞(成熟破骨细胞,mature osteoclast,mOC)数目.结论老鹳草素对维甲酸致大鼠骨质疏松症有对抗作用,明显抑制体外培养OC的生存率可能是抗骨质疏松作用的机制之一.Objective To evaluate the effects of and the survival rate of osteoclasts. Methods During geraniin (Ge) on tretinoin - induced osteoporosis in rats duplicating osteoporotic model in rats induced by tretinoin, the animals were randomly divided into control group, osteoporosis group, Ge and nilestriol treated groups, respectively. All the indexes of bone morphology and metabolism were observed after 1 week of medicine - treatment. The osteoclasts (OCs) isolated mechanically from long bones of SD rats aged one - day were plated in 48 - well plates directly or on ivory bone slices in 24 - well plates for culture together with different concentrations of Ge or 10 - 6 mol/L acetazolamide (Az) . Results Ge administered intragastrically significantly reduced alkaline phosphatase (ALP) in serum, and significantly increased the content of calcium both in serum and bone, the trabecular thickness, and the trabecular area/the field of vision ratio. Ge and Az decreased the total numbers of multinucleated TRAP - positive osteoclasts in cultures. Conclusion 2Ge showed a preventive effect in the model of osteoporotic rats induced by tretinoin. The mechanisms may be closely associated with the inhibition on the survival of osteoclasts.
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