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Objective <p>To observe the regulatory effect of herb-partitioned moxibustion (HPM) on 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced Crohn disease (CD) rats with chronic inflammatory visceral pain (CIVP), aiming to investigate the spinal mechanism of HPM in relieving CIVP.</p> Methods <p>Fifty-four clean-grade male Sprague-Dawley rats were randomly divided into a normal group, a model group, an HPM group, a sham HPM group, a c-Jun N-terminal kinase (JNK) inhibitor group, and a dimethyl sulfoxide (DMSO) solvent group, with 9 rats in each group. The CIVP rat model was induced by TNBS dissolved in 50% ethanol. The HPM group underwent HPM intervention at Tianshu (ST25) and Qihai (CV6); the sham HPM group received the same intervention but without igniting the moxa cones. The JNK inhibitor group received an intrathecal injection of the JNK inhibitor SP600125 between the L<sub>5</sub> and L<sub>6</sub> vertebrae, while the DMSO solvent group was administered equal volumes of 1% DMSO via the same route. Pain-related behaviors were assessed using the abdominal withdrawal reflex (AWR) score, mechanical withdrawal threshold (MWT), and thermal withdrawal latency (TWL). The changes in colon tissue histopathology were examined by hematoxylin-eosin staining. The mRNA expression levels of c-Jun, activating transcription factor 2 (ATF-2), transforming growth factor β-activated kinase 1 (TAK1), mitogen-activated protein kinase kinase (MKK) 4, and MKK7 in the spinal cord were measured by real-time quantitative reverse-transcription polymerase chain reaction, and the phosphorylated protein levels of JNK, c-Jun, ATF-2, TAK1, MKK4, and MKK7 were quantified by Western blotting.</p> Results <p>TNBS-induced CD rats exhibited significantly higher AWR scores, lower MWT and TWL, and increased colonic pathological scores versus normal controls. Furthermore, the phosphorylated protein level of JNK was markedly upregulated, and the mRNA and phosphorylated protein levels of c-Jun, ATF-2, TAK1, MKK4, and MKK7 were markedly upregulated in the spinal cord (<i>P</i>&lt;0.01 or <i>P</i>&lt;0.05). Compared to the model group and the sham HPM group, HPM intervention significantly reduced AWR and colonic pathological scores while increasing MWT and TWL; HPM also significantly downregulated the phosphorylated protein level of JNK, the mRNA and phosphorylated protein levels of c-Jun, ATF-2, TAK1, MKK4, and MKK7 (<i>P</i>&lt;0.01 or <i>P</i>&lt;0.05). No significant differences were found between the HPM and JNK inhibitor groups regarding behavioral scores, colonic pathological scores, or the aforementioned JNK pathway components (<i>P</i>&gt;0.05).</p> Conclusion <p>HPM effectively alleviated CIVP in CD rats. Inhibition of the aberrant activation of the spinal JNK/c-Jun signaling pathway may be one of the key mechanisms underlying the analgesic effects of HPM.</p>

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Herb-partitioned moxibustion alleviates chronic inflammatory visceral pain in Crohn disease rats potentially by inhibiting the spinal JNK/c-Jun pathway

  • 期刊论文

  • 发表日期：

    2026年4月14日

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  • Can Yang,
  • Zhiyuan Li,
  • Yanting Yang,
  • Cuihong Zhang,
  • Lingxiang Wu,
  • Chen Xie,
  • Jie Liu,
  • Jue Hong,
  • Dan Zhang,
  • Xiaopeng Ma

摘要

Objective

To observe the regulatory effect of herb-partitioned moxibustion (HPM) on 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced Crohn disease (CD) rats with chronic inflammatory visceral pain (CIVP), aiming to investigate the spinal mechanism of HPM in relieving CIVP.

Methods

Fifty-four clean-grade male Sprague-Dawley rats were randomly divided into a normal group, a model group, an HPM group, a sham HPM group, a c-Jun N-terminal kinase (JNK) inhibitor group, and a dimethyl sulfoxide (DMSO) solvent group, with 9 rats in each group. The CIVP rat model was induced by TNBS dissolved in 50% ethanol. The HPM group underwent HPM intervention at Tianshu (ST25) and Qihai (CV6); the sham HPM group received the same intervention but without igniting the moxa cones. The JNK inhibitor group received an intrathecal injection of the JNK inhibitor SP600125 between the L5 and L6 vertebrae, while the DMSO solvent group was administered equal volumes of 1% DMSO via the same route. Pain-related behaviors were assessed using the abdominal withdrawal reflex (AWR) score, mechanical withdrawal threshold (MWT), and thermal withdrawal latency (TWL). The changes in colon tissue histopathology were examined by hematoxylin-eosin staining. The mRNA expression levels of c-Jun, activating transcription factor 2 (ATF-2), transforming growth factor β-activated kinase 1 (TAK1), mitogen-activated protein kinase kinase (MKK) 4, and MKK7 in the spinal cord were measured by real-time quantitative reverse-transcription polymerase chain reaction, and the phosphorylated protein levels of JNK, c-Jun, ATF-2, TAK1, MKK4, and MKK7 were quantified by Western blotting.

Results

TNBS-induced CD rats exhibited significantly higher AWR scores, lower MWT and TWL, and increased colonic pathological scores versus normal controls. Furthermore, the phosphorylated protein level of JNK was markedly upregulated, and the mRNA and phosphorylated protein levels of c-Jun, ATF-2, TAK1, MKK4, and MKK7 were markedly upregulated in the spinal cord (P<0.01 or P<0.05). Compared to the model group and the sham HPM group, HPM intervention significantly reduced AWR and colonic pathological scores while increasing MWT and TWL; HPM also significantly downregulated the phosphorylated protein level of JNK, the mRNA and phosphorylated protein levels of c-Jun, ATF-2, TAK1, MKK4, and MKK7 (P<0.01 or P<0.05). No significant differences were found between the HPM and JNK inhibitor groups regarding behavioral scores, colonic pathological scores, or the aforementioned JNK pathway components (P>0.05).

Conclusion

HPM effectively alleviated CIVP in CD rats. Inhibition of the aberrant activation of the spinal JNK/c-Jun signaling pathway may be one of the key mechanisms underlying the analgesic effects of HPM.