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人甲状旁腺激素 1-34 间断治疗 SAMP6 快速老化小鼠的效果。

Effect of intermittent treatment with human Parathyroid Hormone 1-34 in SAMP6 senescence-accelerated mice.

机构信息

Department of Orthopedic Surgery, Fujita Health University, Toyoake City, Aichi, Japan.

出版信息

J Endocrinol Invest. 2010 Jun;33(6):395-400. doi: 10.1007/BF03346610. Epub 2009 Nov 12.

Abstract

We examined trabecular and cortical bone in the senescence-accelerated mouse prone 6 (SAMP6) murine model of senile osteoporosis after treatment with human PTH 1-34. Sixteen-week-old female SAMP6 mice were assigned to control and PTH groups. PTH (20 microg/kg) was administered sc 3 times a week for 12 weeks. The control mouse strain, senescence-accelerated mouse resistant 1 (SAMR1), was used for comparison. The femoral metaphysis and diaphysis were used to measure bone mineral density (BMD), analyze the trabecular and the cortical structure by micro-computed tomography, and for conducting the bone strength test. PTH significantly attenuated the loss of BMD, improved the trabecular bone microstructure, and increased the bone strength in the femoral metaphysis. We did not find any differences in the bone strength of the femoral diaphysis after PTH treatment, although the cortical bone volume and cortical thickness were improved. Although the cortical thickness increased, the cortical bone density decreased, likely because of the increase of cortical porosity in the distal metaphysis after administration of PTH.

摘要

我们研究了经人甲状旁腺激素 1-34 治疗后的衰老加速模型 6 号(SAMP6)小鼠的骨小梁和皮质骨,该模型是老年性骨质疏松症的动物模型。将 16 周龄的雌性 SAMP6 小鼠分配到对照组和 PTH 组。PTH(20 微克/千克)每周皮下注射 3 次,共 12 周。使用衰老加速抵抗 1 号(SAMR1)作为对照小鼠品系进行比较。使用股骨干骺端和骨干来测量骨密度(BMD),通过微计算机断层扫描分析骨小梁和皮质结构,并进行骨强度测试。PTH 显著减少了 BMD 的丢失,改善了骨小梁微结构,并增加了股骨干骺端的骨强度。我们没有发现 PTH 治疗后股骨骨干的骨强度有任何差异,尽管皮质骨体积和皮质厚度有所改善。尽管皮质厚度增加,但皮质骨密度下降,这可能是由于 PTH 给药后远端干骺端皮质孔隙度增加所致。

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