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三七皂苷通过降低腰椎不稳小鼠的终板孔隙率来减轻椎间盘退变。

Panax notoginseng saponins attenuate intervertebral disc degeneration by reducing the end plate porosity in lumbar spinal instability mice.

作者信息

Hu Hao, Chen Yan, Huang Fangli, Chen Bolin, Zou Zhiyuan, Tan Bizhi, Yi Hualin, Liu Chun, Wan Yong, Ling Zemin, Zou Xuenong

机构信息

Department of Spine Surgery and Guangdong Provincial Key Laboratory of Orthopaedics and Traumatology Sun Yat-sen University First Affiliated Hospital Guangzhou China.

Precision Medicine Institute Sun Yat-sen University First Affiliated Hospital Guangzhou China.

出版信息

JOR Spine. 2021 Nov 30;4(4):e1182. doi: 10.1002/jsp2.1182. eCollection 2021 Dec.

DOI:10.1002/jsp2.1182
PMID:35005448
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8717113/
Abstract

Although painkillers could alleviate some of the symptoms, there are no drugs that really cope with the intervertebral disc degeneration (IDD) at present, so it is urgent to find a cure that could prevent or reverse the progression of IDD. During the development of IDD, the cartilaginous end plates (EPs) become hypertrophic and porous by the increase of osteoclast activities, which hinder the penetration of nutrition. The compositional and structural degeneration of the EP may cause both nutritional as well as mechanical impairment to the nucleus pulposus (NP) so that developing drugs that target the degenerating EP may be another option in addition to targeting the NP. In the lumbar spine instability mouse model, we found increased porosity in the cartilaginous EP, accompanied by the decrease in total intervertebral disc volume. Panax notoginseng saponins (PNS), a traditional Chinese patent drug with anti-osteoclastogenesis effect, could alleviate IDD by inhibiting aberrant osteoclast activation in the porous EP. Further in vitro experiment validated that PNS inhibit the receptor activator of nuclear factor kappa-Β ligand-induced osteoclast differentiation, while the transcriptional activation of PAX6 may be involved in the mechanism, which had been defined as an inhibitory transcription factor in osteoclastogenesis. These findings may provide a novel therapeutic strategy for IDD.

摘要

尽管止痛药可以缓解一些症状,但目前尚无真正能应对椎间盘退变(IDD)的药物,因此迫切需要找到一种能够预防或逆转IDD进展的治疗方法。在IDD发展过程中,软骨终板(EP)因破骨细胞活性增加而变得肥厚且多孔,这阻碍了营养物质的渗透。EP的成分和结构退变可能会对髓核(NP)造成营养和机械损伤,因此开发针对退变EP的药物可能是除了针对NP之外的另一种选择。在腰椎不稳小鼠模型中,我们发现软骨EP的孔隙率增加,同时椎间盘总体积减小。三七总皂苷(PNS)是一种具有抗破骨细胞生成作用的传统中成药,可通过抑制多孔EP中异常的破骨细胞活化来缓解IDD。进一步的体外实验证实,PNS可抑制核因子κB受体活化因子配体诱导的破骨细胞分化,而PAX6的转录激活可能参与了该机制,PAX6在破骨细胞生成中被定义为一种抑制性转录因子。这些发现可能为IDD提供一种新的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c54/8717113/c1d6fb590bf8/JSP2-4-e1182-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c54/8717113/2b6195fde475/JSP2-4-e1182-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c54/8717113/f14cbf7ff648/JSP2-4-e1182-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c54/8717113/4485930b7dee/JSP2-4-e1182-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c54/8717113/234583978263/JSP2-4-e1182-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c54/8717113/b118ebce8cda/JSP2-4-e1182-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c54/8717113/c1d6fb590bf8/JSP2-4-e1182-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c54/8717113/2b6195fde475/JSP2-4-e1182-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c54/8717113/f14cbf7ff648/JSP2-4-e1182-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c54/8717113/4485930b7dee/JSP2-4-e1182-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c54/8717113/234583978263/JSP2-4-e1182-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c54/8717113/b118ebce8cda/JSP2-4-e1182-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c54/8717113/c1d6fb590bf8/JSP2-4-e1182-g004.jpg

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