果硼酸钙通过 DDIT3 激活刺猬信号改善大鼠膝骨关节炎

IF 3.4 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
TingXin Yan, Peng Wang, Zhilin Cao
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引用次数: 0

摘要

CFB治疗膝骨关节炎的机制尚不清楚,值得进一步探讨。通过TNF-α刺激C28/I2细胞,构建MIA诱导的OA大鼠模型,然后用一定浓度的CFB处理。评估了 CFB 对软骨细胞凋亡、炎症反应和胶原基质降解的影响。此外,我们还通过 Western 印迹分析了 CFB 对 DDIT3 和 Hedgehog 通路的调控。应用平滑激动剂抑制剂SAG和DDIT3过表达慢病毒研究了CFB如何调控DDIT3和Hedgehog通路以保护骨关节炎。实验结果证明了CFB对TNF-α刺激的C28/I2细胞具有保护作用。在TNF-α刺激的C28/I2细胞中,CFB处理可下调DDIT3蛋白并使HH通路失活,这种效应可能与DDIT3或HH通路有关。此外,CFB 对 HH 通路的抑制作用与 DDIT3 有关。体内动物实验表明,CFB能抑制关节炎大鼠软骨胶原基质降解、抑制软骨细胞凋亡、改善软骨细胞损伤、缓解疼痛,而CFB对OA大鼠的作用与DDIT3介导的HH通路有关。总之,CFB 对骨关节炎有明显的治疗作用,能保护软骨降解和损伤,抑制炎症反应。DDIT3 可能作为中间分子参与了该药物对 OA 的保护作用。CFB通过DDIT3调节SHH/GLi1通路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Calcium Fructoborate Improves Knee Osteoarthritis in Rats by Activating Hedgehog Signaling Through DDIT3.

The mechanism of CFB in treating knee osteoarthritis is not yet clear and deserves further discussion. The C28/I2 cell was stimulated by TNF-α and the MIA-induced OA rat model were constructed, and then treated with a certain concentration of CFB. The effects of CFB on chondrocyte apoptosis, inflammatory response, and collagen matrix degradation were assessed. Furthermore, we analyzed the regulation of CFB on the DDIT3 and Hedgehog pathways through western blot analysis. The smoothened agonist inhibitor SAG and DDIT3 overexpression lentivirus were applied to investigate how CFB regulates DDIT3 and Hedgehog pathway to protect against osteoarthritis. Our experimental results proved the protective of CFB against TNF-α stimulated C28/I2 cells. CFB treatment downregulated the DDIT3 protein and inactivated the HH pathway in TNF-α stimulated C28/I2 cells, and this effect may be related to the DDIT3 or HH pathway. Furthermore, the inhibitory effect of CFB on the HH pathway is related to DDIT3. In vivo animal assays showed that CFB can inhibit the degradation of cartilage collagen matrix, inhibit chondrocyte apoptosis, improve chondrocyte damage, and alleviate pain in arthritis rats, and the effect of CFB on OA rats is related to the HH pathway mediated by DDIT3. In summary, CFB has significant therapeutic effects on osteoarthritis, protecting cartilage degradation and damage, and inhibiting inflammatory responses. DDIT3 may participate as an intermediate molecule in the protective effect of the drug on OA. The SHH/GLi1 pathway is regulated by CFB through DDIT3.

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来源期刊
Biological Trace Element Research
Biological Trace Element Research 生物-内分泌学与代谢
CiteScore
8.70
自引率
10.30%
发文量
459
审稿时长
2 months
期刊介绍: Biological Trace Element Research provides a much-needed central forum for the emergent, interdisciplinary field of research on the biological, environmental, and biomedical roles of trace elements. Rather than confine itself to biochemistry, the journal emphasizes the integrative aspects of trace metal research in all appropriate fields, publishing human and animal nutritional studies devoted to the fundamental chemistry and biochemistry at issue as well as to the elucidation of the relevant aspects of preventive medicine, epidemiology, clinical chemistry, agriculture, endocrinology, animal science, pharmacology, microbiology, toxicology, virology, marine biology, sensory physiology, developmental biology, and related fields.
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