Baicalin alleviates intervertebral disc degeneration by inhibiting the p38 MAPK signaling pathway

IF 3.9

Experimental gerontology Pub Date : 2025-03-31 DOI:10.1016/j.exger.2025.112743

Yating Wu , Fengrui Li , Shibin Shu , Zhenhua Feng , Yong Qiu , Sen Li , Zezhang Zhu

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Abstract

Background

Intervertebral disc degeneration (IVDD) represents a prevalent degenerative pathology of the spinal, primarily precipitated by inflammatory processes and the deterioration of extracellular matrix (ECM). Baicalin has an effective anti-inflammatory effect on degenerative diseases. In addition, the P38 mitogen-activated protein kinase (MAPK) signaling pathway plays a crucial role in the pathogenesis of IVDD.

Objective

To investigate the therapeutic potential of baicalin in modulating pathological changes in IVDD.

Methods

To design an in vitro model of degeneration of nucleus pulposus cells (NPCs) stimulated by IL-1β and an in vivo mouse model of needling to assess the protective effect of baicalin against IVDD and its underlying mechanism.

Results

Baicalin down-regulated inflammatory factors (INOS, COX-2, IL-6) and catabolic factors (MMP-3, MMP-13, ADAMTS-5) while up-regulating anabolic factors (collagen II, SOX-9) by inhibiting the activation of the p38 MAPK signaling pathway, in addition to slowing down the progression of IVDD in the mouse acupuncture model.

Conclusion

Our study demonstrated in vitro experiments that baicalin attenuates IL-1β-stimulated IVDD by inhibiting activation of the P38 MAPK signaling pathway. Meanwhile, the effects of baicalin were also confirmed in vivo experiments, Consequently, we propose that baicalin is a promising therapeutic agent for the treatment of disc degeneration.

Abstract Image

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黄芩苷通过抑制p38 MAPK信号通路减轻椎间盘退变。

背景：椎间盘退变（IVDD）是一种常见的脊柱退行性病理，主要由炎症过程和细胞外基质（ECM）的恶化引起。黄芩苷对退行性疾病有有效的抗炎作用。此外，P38丝裂原活化蛋白激酶（MAPK）信号通路在IVDD的发病机制中起着至关重要的作用。目的：探讨黄芩苷对IVDD病理改变的调节作用。方法：建立IL-1β刺激髓核细胞（NPCs）变性的体外模型和针刺小鼠模型，探讨黄芩苷对IVDD的保护作用及其机制。结果：黄芩苷通过抑制p38 MAPK信号通路的激活，下调炎症因子（INOS、COX-2、IL-6）和分解代谢因子（MMP-3、MMP-13、ADAMTS-5），上调合成代谢因子（collagen II、SOX-9），并减缓针刺小鼠IVDD的进展。结论：体外实验证明黄芩苷通过抑制P38 MAPK信号通路的激活来减轻il -1β刺激的IVDD。同时，体内实验也证实了黄芩苷的作用，因此，我们认为黄芩苷是一种很有前景的治疗椎间盘退变的药物。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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