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高车前素通过减轻肿瘤坏死因子-α诱导的髓核细胞衰老和炎症,对椎间盘退变发挥治疗作用。

Homoplantaginin exerts therapeutic effects on intervertebral disc degeneration by alleviating TNF-α-induced nucleus pulposus cell senescence and inflammation.

作者信息

Guo Jiadong, Zhang Pu, Yang Xiao, Wang Xin, Cao Xiankun, Zhao Jie

机构信息

Shanghai Key Laboratory of Orthopedic Implants, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.

出版信息

Front Pharmacol. 2025 Mar 27;16:1526107. doi: 10.3389/fphar.2025.1526107. eCollection 2025.

Abstract

The incidence of intervertebral disc degeneration (IDD) is increasing year by year, while the age of onset of IDD is decreasing year by year. For the individuals affected by IDD, an alternative treatment to surgery is required. IDD is thought to be related to nucleus pulposus (NP) cell senescence and inflammation. Therefore, inhibition of NP cell inflammation and senescence may counteract IDD. We screened 20 small-molecule drugs to compare their anti-inflammatory effects, and finally selected homoplantaginin (HPG) as a treatment regimen. HPG is an extract of with anti-inflammatory properties. The objective of this research was to investigate if HPG could have a therapeutic effect on IDD through its anti-inflammatory or anti-aging effects. We identified the appropriate concentration of HPG in primary NP cell cultures and demonstrated that it inhibited inflammatory pathway activation and reduced the senescence phenotype of NP cells . And , the therapeutic effect of HPG on caudal disc degeneration was confirmed consistently. In conclusion, our findings suggest that HPG can alleviate the degeneration in the pathogenesis of IDD and that it has a potential effect in the treatment of IDD.

摘要

椎间盘退变(IDD)的发病率逐年上升,而IDD的发病年龄却逐年下降。对于受IDD影响的个体,需要一种替代手术的治疗方法。IDD被认为与髓核(NP)细胞衰老和炎症有关。因此,抑制NP细胞炎症和衰老可能会对抗IDD。我们筛选了20种小分子药物以比较它们的抗炎作用,最终选择高车前素(HPG)作为治疗方案。HPG是一种具有抗炎特性的提取物。本研究的目的是调查HPG是否能通过其抗炎或抗衰老作用对IDD产生治疗效果。我们在原代NP细胞培养物中确定了HPG的合适浓度,并证明它能抑制炎症途径激活并减少NP细胞的衰老表型。并且,HPG对尾椎间盘退变的治疗效果也得到了一致证实。总之,我们的研究结果表明,HPG可以减轻IDD发病机制中的退变,并且在IDD治疗中具有潜在作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fe1/11983561/2930d6d9b5a7/fphar-16-1526107-g001.jpg

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