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出 处:《中华中医药学刊》2013年第12期2623-2627,共5页Chinese Archives of Traditional Chinese Medicine
基 金:国家自然科学青年基金资助项目(81302879);辽宁省博士启动基金资助项目(20101068)
摘 要:目的:研究糖皮质激素性骨质疏松症大鼠骨组织中OPG/RANKL的mRNA和蛋白表达,揭示糖皮质激素骨质疏松症的发病机理,阐述纳米钙补肾中药的调节作用机制。方法:用糖皮质激素注射的方法复制骨质疏松症模型,用纳米钙及具有益肾填精、补钙壮骨作用的补肾中药高、低剂量对实验大鼠治疗8周,以骨疏康颗粒、盖天力钙片作为阳性对照组,正常大鼠和模型空白组为空白对照组。用PCR法、Western印迹法检测骨质疏松症大鼠骨组织中OPG/RANKLmRNA和蛋白表达。结果:正常大鼠骨组织可以在基因、蛋白水平表达OPG及RANKL,表明正常骨组织中存在OPG/RANK/RANKL系统,此系统可能在骨组织维持骨密度的作用上发挥重要的作用。糖皮质激素可影响骨组织中OPG/RANK/RANKL系统,促进破骨细胞的分化抑制成骨细胞的形成,从而影响骨形成诱发骨质疏松症。结论:纳米钙补肾中药通过调控大鼠骨组织中OPG/RANKL mRNA和蛋白表达,可缓解糖皮质激素对骨组织中OPG/RANK/RANKL系统的影响。抑制破骨细胞的分化,促进成骨细胞的形成,从而对糖皮质激素性骨质疏松症有一定的防治作用。Objective :To study expressions of OPG/RANKL mRNA and protein of the bone tissue in kidney deficiency rats with osteoporosis induced by glucocorticoid. To reveal the pathogenesis of osteoporosis. To explore the mechanism of the adjustable function of nanometer calcium kidney - tonifying Chinese herbs. Methods : The method of glucocorticoid in- jection was used. We established the rat model of osteoporosis due to kidney - deficiency. The osteoporosis rats with ex- perimental drugs (high, low dose group) were treated for 8 weeks, which was notifying kidney to consolidate the essence and strengthening bone and marrow, invigorating kidney to make the bone strong. Simultaneously, Gushukang granule and Gaitianli tablets were used as positive control groups. And rats in the normal group and model group were not given any treatment. We had used the PCR method and Western blotting method to detect the expression of OPG/RANKL RNA and proteins in the bone of the rats. Results : Normal rat bone tissue can express OPG/RANKL in gene and protein level, which is important for helping to maintain bone mineral density. The occurrence of rats osteoporosis caused by glucocorticoids is related with the change of bone tissue OPG/RANKL mRNA and the protein expression, affecting bone formation. Conclu- sions : Nanometer calcium kidney - tonifying Chinese herbs can control OPG/RANKL mRNA and protein expression in rat bone tissue, inhibit osteoclast differentiation, promote the formation of osteoblast, and thus prevent and control the glu- cocorticoids - induced osteoporosis.
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