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Objective <p>To investigate the roles of the mechanically-sensitive channel Piezo1 and the inflammatory factor IL-6 in cervical spondylotic radiculopathy (CSR) pain and the mechanism between them.</p> Methods <p>The CSR model in SD rats was established by nerve injury caused by steel needle compression. Immunocytochemistry, double-fluorescence labeling and behavioral tests were used to analyze the expression and co-localization of Piezo1 and IL-6. Interventions were carried out using Yoda1 (Piezo channel activator) and and Dooku1 (specific antagonist of the Piezo1 agonist Yoda1), and the changes in mechanical pain threshold and thermal pain threshold were evaluated.</p> Results <p>In the dorsal root ganglia of the compressed segments of CSR model rats, the expressions of Piezo1 and IL-6 were significantly up-regulated. 74.3% of Piezo1-positive neurons co-expressed IL-6, and both of them were mainly distributed in type C (IB4 + /CGRP +) and type A (NF200 +) neurons.In Sham rats, intrathecal administration of Yoda1 or Dooku1 did not cause significant changes in pain thresholds or IL-6 expression (<i>P</i> &gt; 0.05). Yoda1 significantly increased IL-6 expression and induced hyperalgesia in CSR model rats (<i>p</i> &lt; 0.05), while the Vehicle group showed no such effects. Notably, Dooku1 intervention reversed the effects of Yoda1: after pretreatment with Yoda1 in CSR rats, subsequent Dooku1 administration significantly reduced IL-6 expression and increased mechanical/thermal pain thresholds (<i>p</i> &lt; 0.05).</p> Conclusion <p>Piezo1 is involved in the occurrence of radicular pain in CSR by regulating the expression of IL-6, and this effect is dependent on the pathological microenvironment of CSR. Targeting the Piezo1/IL-6 signaling pathway may provide a new direction for the non-invasive treatment of radicular pain.</p> Graphical Abstract <p></p>

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Effects of Piezo1/IL-6 on radicular pain in cervical spondylotic radiculopathy

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月24日

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  • Haibao Wen,
  • Daiyuan Liu,
  • Changxiao Han,
  • Minrui Fu,
  • Jing Li,
  • Guangwei Liu,
  • Liguo Zhu,
  • Minshan Feng

摘要

Objective

To investigate the roles of the mechanically-sensitive channel Piezo1 and the inflammatory factor IL-6 in cervical spondylotic radiculopathy (CSR) pain and the mechanism between them.

Methods

The CSR model in SD rats was established by nerve injury caused by steel needle compression. Immunocytochemistry, double-fluorescence labeling and behavioral tests were used to analyze the expression and co-localization of Piezo1 and IL-6. Interventions were carried out using Yoda1 (Piezo channel activator) and and Dooku1 (specific antagonist of the Piezo1 agonist Yoda1), and the changes in mechanical pain threshold and thermal pain threshold were evaluated.

Results

In the dorsal root ganglia of the compressed segments of CSR model rats, the expressions of Piezo1 and IL-6 were significantly up-regulated. 74.3% of Piezo1-positive neurons co-expressed IL-6, and both of them were mainly distributed in type C (IB4 + /CGRP +) and type A (NF200 +) neurons.In Sham rats, intrathecal administration of Yoda1 or Dooku1 did not cause significant changes in pain thresholds or IL-6 expression (P > 0.05). Yoda1 significantly increased IL-6 expression and induced hyperalgesia in CSR model rats (p < 0.05), while the Vehicle group showed no such effects. Notably, Dooku1 intervention reversed the effects of Yoda1: after pretreatment with Yoda1 in CSR rats, subsequent Dooku1 administration significantly reduced IL-6 expression and increased mechanical/thermal pain thresholds (p < 0.05).

Conclusion

Piezo1 is involved in the occurrence of radicular pain in CSR by regulating the expression of IL-6, and this effect is dependent on the pathological microenvironment of CSR. Targeting the Piezo1/IL-6 signaling pathway may provide a new direction for the non-invasive treatment of radicular pain.

Graphical Abstract