التفاصيل البيبلوغرافية
| العنوان: |
Vitamin D delays intervertebral disc degeneration and improves bone quality in ovariectomized rats. |
| المؤلفون: |
Xu, Hao‐Wei, Fang, Xin‐Yue, Chen, Hao, Zhang, Shu‐Bao, Yi, Yu‐Yang, Ge, Xiao‐Yong, Liu, Xiao‐Wei, Wang, Shan‐Jin |
| المصدر: |
Journal of Orthopaedic Research; Jun2024, Vol. 42 Issue 6, p1314-1325, 12p |
| مصطلحات موضوعية: |
INTERVERTEBRAL disk, VITAMIN D, BONE density, NUCLEUS pulposus, OXIDANT status, VERTEBRAE, LUMBAR vertebrae |
| مستخلص: |
Known to be involved in bone‐cartilage metabolism, Vitamin D (VD) may play a role in human's disc pathophysiology. Given that postmenopausal women are prone to suffer VD deficiency and intervertebral disc degeneration (IDD), this study is intended to investigate whether VD can delay IDD in ovariectomized rats by improving bone microstructure and antioxidant stress. Female Sprague–Dawley rats were randomly allocated into four groups: sham, oophorectomy (OVX)+VD deficiency (VDD), OVX, and OVX+VD supplementation (VDS). In vivo, after a 6‐month intervention, imaging and pathology slice examinations showed that IDD induced by OVX was significantly alleviated in VDS and deteriorated by VDD. The expressions of aggrecan and Collagen II in intervertebral disc were reduced by OVX and VDD, and elevated by VDS. Compared with the OVX+VDD and OVX group vertebrae, OVX+VDS group vertebrae showed significantly improved endplate porosity and lumbar bone mineral density with increased percent bone volume and trabecular thickness. Furthermore, 1α,25(OH)2D3 restored the redox balance (total antioxidant capacity, ratio of oxidized glutathione/glutathione) in the disc. The cocultivation of 1α,25(OH)2D3 and nucleus pulposus cells (NPCs) was conducted to observe its potential ability to resist excessive oxidative stress damage induced by H2O2. In vitro experiments revealed that 1α,25(OH)2D3 reduced the senescence, apoptosis, and extracellular matrix degradation induced by H2O2 in NPCs. In conclusion, VDS exhibits protective effects in OVX‐induced IDD, partly by regulating the redox balance and preserving the microstructure of endplate. This finding provides a new idea for the prevention and treatment of IDD. [ABSTRACT FROM AUTHOR] |
|
Copyright of Journal of Orthopaedic Research is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) |
| قاعدة البيانات: |
Complementary Index |
Full Text Finder