摘要
目的以去势大鼠建立绝经后骨质疏松模型,探讨氨基胍(aminoguanidine)溶液对绝经后骨质疏松症骨形成的刺激作用和药理机制。方法54只SD大鼠随机分为3组:去势后给药实验组(groups1,G1)、单纯去势组(G2)和对照组(G3),并将术后第4、10和16周定为实验周。观测骨形成指标:骨钙素(BGP)、骨特异性碱性磷酸酶(骨AKP)和总碱性磷酸酶(总AKP)和骨吸收指标:尿吡啶醚(PYD)和脱氧吡啶醚(DPD),同步用IBAS计算机全自动图像分析系统对不脱钙骨组织动态观测骨形态计量学参数。结果给药实验组在去势后4￣16周BGP和骨AKP明显高于单纯去势组(分别为P<0.01和P<0.05)。而骨吸收指标:尿PYD和DPD2组之间差异无显著性(P>0.05)。骨形成表面(FS)和骨小梁体积(TBV),骨小梁平均厚度(MTT)较单纯去势组明显升高,尤其是TBV和FS(分别为P<0.001和P<0.01),这种差异在第10周最为显著。随着给药时间的延长(第16周)MAR逐渐增加(P<0.001)。骨吸收表面(RS)与单纯去势组比较在所有实验周均无差异。结论氨基胍可刺激骨质疏松大鼠成骨细胞活跃增生,促进骨转换速率,并可使骨质疏松症骨组织形态改善。
[Objective] To explore the dynamic changes effects by aminoguanidine solution on histomorphometry of postmenopausol osteoporosis with stimulation on bone formation,to study the pharmacal mechanism of aminoguanidine. [Methods] Fifty-four female Sprague-dawly rats were randomly divided into 3 groups： treatment group with aminoguanidine （group 1, G1） and ovariectomized group （G2） and sham-ov （G3）. Laboratory week was hypothesized by within 4-16 weeks： 4 weeks,10 weeks and 16 weeks later after operation. Observed bone formation signalize： bone osteocalin （BGP）; serum bone specific alkeliphosphatase （bone AKP） and total alkaliphosphatase （AKP）, it was bone formation parameters, and bone resorption indices：urine pyridinolin （PYD） and deoxypyridinoline （DPD） were determined. At the same time, bone histomorphometry was measured with whole automobile imaging analysis system. [Results] By the 4-16 weeks after administration, BGP and bone AKP began to increase in G1, compared with G2 was improved significantly （respective P 〈0.01 and P 〈0.05）, but the PYD and DPD respectively level in urine were not significantly decreased between in G1 than in G2 （P 〉0.05）, and bony histomorphometry began to change gradually 4-16 weeks in G1, bone formation signal such as trabecular bone volume （TBV） and formation surfase （FS） of G1 increased significantly than those of G2, this difference was most obvious at 10 week. The in- crease of MAR was in a time-dependant manner. [Conclusions] The aminoguanidine could stimulate active hyperplasia of bone cell and mainly influences for increased of bone formation which might prevent ovariectomized rat from bone loss by repressing the advanced glycosylation end products（AGES）, lead to improve the shape of the bone in osteoporosis.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2006年第4期497-500,共4页
China Journal of Modern Medicine
基金
湖北省教育厅重点项目资助(No:2004D007)
关键词
氨基胍
骨质疏松症
骨形成
aminoguanidine
osteoporosis
bone formation
