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硒酸钠治疗可减轻大鼠创伤性脑损伤后骨量的减少。

Sodium selenate treatment mitigates reduction of bone volume following traumatic brain injury in rats.

作者信息

Brady R D, Grills B L, Romano T, Wark J D, O'Brien T J, Shultz S R, McDonald S J

机构信息

Department of Physiology, Anatomy and Microbiology, La Trobe University, VIC, 3086, Australia.

出版信息

J Musculoskelet Neuronal Interact. 2016 Dec 14;16(4):369-376.

PMID:27973389
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5259578/
Abstract

OBJECTIVES

Administration of sodium selenate to rats given traumatic brain injury (TBI) attenuates brain damage and improves long-term behavioural outcomes. We have previously provided evidence that TBI causes bone loss in rats, however the effect of sodium selenate treatment on bone quantity following TBI is unknown.

METHODS

Rats were randomly assigned into sham injury or fluid percussion injury (FPI) groups and administered saline or sodium selenate for 12 weeks post-injury. Femora were analysed using histomorphometry, peripheral quantitative computed tomography (pQCT) and biomechanical testing.

RESULTS

Distal metaphyseal trabecular bone volume fraction of FPI-selenate rats was higher than FPI-vehicle rats (41.8%; p<0.01), however, femora from selenate-treated groups were shorter in length (4.3%; p<0.01) and had increased growth plate width (22.1%; p<0.01), indicating that selenate impaired long bone growth. pQCT analysis demonstrated that distal metaphyseal cortical thickness was decreased in TBI rats compared to shams (11.7%; p<0.05), however selenate treatment to TBI animals offset this reduction (p<0.05). At the midshaft we observed no differences in biomechanical measures.

CONCLUSION

These are the first findings to indicate that mitigating TBI-induced neuropathology may have the added benefit of preventing osteoporosis and associated fracture risk following TBI.

摘要

目的

给创伤性脑损伤(TBI)大鼠施用硒酸钠可减轻脑损伤并改善长期行为结果。我们之前已证明TBI会导致大鼠骨质流失,然而,硒酸钠治疗对TBI后骨量的影响尚不清楚。

方法

将大鼠随机分为假损伤组或液压冲击伤(FPI)组,并在损伤后12周给予生理盐水或硒酸钠。使用组织形态计量学、外周定量计算机断层扫描(pQCT)和生物力学测试对股骨进行分析。

结果

FPI-硒酸钠组大鼠远端干骺端小梁骨体积分数高于FPI-载体组大鼠(41.8%;p<0.01),然而,硒酸钠治疗组的股骨长度较短(4.3%;p<0.01),生长板宽度增加(22.1%;p<0.01),表明硒酸钠损害了长骨生长。pQCT分析表明,与假手术组相比,TBI大鼠远端干骺端皮质厚度降低(11.7%;p<0.05),然而,对TBI动物进行硒酸钠治疗可抵消这种降低(p<0.05)。在骨干中部,我们观察到生物力学测量无差异。

结论

这些是首次表明减轻TBI诱导的神经病理学可能具有预防TBI后骨质疏松症和相关骨折风险的额外益处的研究结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49d6/5259578/523e9183917a/JMNI-16-369-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49d6/5259578/6487824576f7/JMNI-16-369-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49d6/5259578/a5c219c0733b/JMNI-16-369-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49d6/5259578/523e9183917a/JMNI-16-369-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49d6/5259578/6487824576f7/JMNI-16-369-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49d6/5259578/a5c219c0733b/JMNI-16-369-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49d6/5259578/523e9183917a/JMNI-16-369-g003.jpg

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