Shen Lin, Ma Chen, Shuai Bo, Yang Yanping
Department of Integrated Traditional Chinese and Western Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.
Exp Ther Med. 2017 Jun;13(6):3297-3304. doi: 10.3892/etm.2017.4404. Epub 2017 Apr 28.
Active vitamin D is closely related to the circulating renin-angiotensin system (RAS) in experimental animal models and humans; however, corresponding local bone data remain limited. The present study examined whether 1,25-dihydroxyvitamin D supplementation altered local bone RAS elements in a murine model of glucocorticoid-induced osteoporosis (GIOP). A total of 36 8-week-old mice were randomized into three equal-sized groups: The sham, GIOP and 1,25-dihydroxyvitamin D treatment groups. After 12 weeks, the cancellous bone microstructure of the third lumbar vertebra and left femur from the mice from each group were examined using micro-computed tomography. To access the impact of glucocorticoid use, the effect of 1,25-dihydroxyvitamin D on cancellous bone microstructure, the expression of bone turnover markers, circulation and expression of the main RAS components was assessed. Results demonstrated that bone volume fraction, trabecular number and trabecular thickness of the treatment and sham groups were significantly higher than the GIOP group (P<0.05). Furthermore, the structure model index, trabecular separation and bone surface to bone volume ratio of the sham and treatment groups were significantly reduced compared with the GIOP group (P<0.05). All assessed parameters exhibited no significant differences between the treatment and sham groups. mRNA expression levels of local bone angiotensin type 1 and 2 receptors and receptor activator of nuclear factor-κB ligand were significantly lower in the treatment group than in the GIOP group (P<0.05); however, there were no significant differences in circulating protein levels between the groups (P>0.05). In conclusion, 1,25-dihydroxyvitamin D may modulate bone metabolism by downregulating the local bone RAS in mice with GIOP.
在实验动物模型和人类中，活性维生素D与循环肾素-血管紧张素系统（RAS）密切相关；然而，相应的局部骨骼数据仍然有限。本研究探讨了补充1,25-二羟基维生素D是否会改变糖皮质激素诱导的骨质疏松症（GIOP）小鼠模型中的局部骨骼RAS成分。总共36只8周龄小鼠被随机分为三个等大小的组：假手术组、GIOP组和1,25-二羟基维生素D治疗组。12周后，使用微型计算机断层扫描检查每组小鼠第三腰椎和左股骨的松质骨微观结构。为了评估糖皮质激素使用的影响，评估了1,25-二羟基维生素D对松质骨微观结构、骨转换标志物表达、主要RAS成分的循环和表达的影响。结果表明，治疗组和假手术组的骨体积分数、小梁数量和小梁厚度显著高于GIOP组（P<0.05）。此外，与GIOP组相比，假手术组和治疗组的结构模型指数、小梁间距和骨表面积与骨体积比显著降低（P<0.05）。治疗组和假手术组之间所有评估参数均无显著差异。治疗组局部骨骼血管紧张素1型和2型受体以及核因子-κB受体激活剂配体的mRNA表达水平显著低于GIOP组（P<0.05）；然而，各组之间循环蛋白水平无显著差异（P>0.05）。总之，1,25-二羟基维生素D可能通过下调GIOP小鼠的局部骨骼RAS来调节骨代谢。
