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Peer-reviewedCC BY 4.0Frontiers in Pharmacology

Emodin attenuates CFA-induced inflammatory pain in association with suppression of the Cx3cl1/Cx3cr1/p38 MAPK signaling axis

  • Xiang Zheng1
  • Jiabao Dai2
  • Changyuan Mao1
  • Weidong Zhang1
  • Jing Huang1
  • Shuqin Hu3
  1. 1Department of Pain Medicine, The Second People’s Hospital of Changzhou, the Third Affiliated Hospital of Nanjing Medical University
  2. 2Department of Anesthesiology, The Second People’s Hospital of Changzhou, the Third Affiliated Hospital of Nanjing Medical University
  3. 3Department of Pediatrics, The Second People’s Hospital of Changzhou, the Third Affiliated Hospital of Nanjing Medical University
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Abstract

Objectives: To investigate the analgesic effect of emodin on Complete Freund’s Adjuvant (CFA)-induced inflammatory pain and to clarify the underlying molecular mechanism.

Methods: Emodin was administered intraperitoneally or prophylactically to attenuate CFA-induced inflammatory pain. RNA-seq was performed to identify the biological functions of differentially expressed genes in mouse dorsal root ganglion (DRG) tissues. The expression levels of Cx3cl1/Cx3cr1 were evaluated by RT-qPCR, Western blotting, and immunofluorescence. Pharmacological and genetic approaches were employed to block Cx3cr1 and assess its effect on pain thresholds in CFA-treated mice. Hematoxylin and eosin (H&E) staining was used to examine the infiltration of immune and inflammatory cells in dorsal root ganglion (DRG) tissues before and after emodin treatment. Following emodin treatment, the levels of p-p38/p38 in DRG tissues were determined by Western blotting, and the mRNA levels of the pro-inflammatory cytokines Tnf-α , Il-1β , and Il-6 in DRG tissues were measured by RT-qPCR.

Results: Both therapeutic and prophylactic administration of emodin effectively alleviated CFA-induced mechanical and thermal hypersensitivity. Emodin treatment suppressed the CFA-induced upregulation of Cx3cl1/Cx3cr1 mRNA and protein levels in the DRG. Pharmacological and genetic blockade of Cx3cr1 effectively attenuated CFA-induced hyperalgesia. In addition, emodin markedly inhibited p-p38/p38 protein expression in the DRG of mice with CFA-induced inflammatory pain, reduced immune cell infiltration in DRG tissues, and downregulated the levels of the pro-inflammatory cytokines Tnf-α , Il-1β , and Il-6 .

Conclusion: Emodin attenuated CFA-induced inflammatory pain in mice, an effect associated with reduced Cx3cl1/Cx3cr1 signaling, decreased p38 MAPK activation, diminished immune-cell infiltration in the DRG, and lower expression of the proinflammatory cytokines Tnf-α , Il-1β , and Il-6 in DRG tissue.

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Cite

BibTeXRIS
BibTeX
@article{zheng2026emodin,
  title = {{Emodin attenuates CFA-induced inflammatory pain in association with suppression of the Cx3cl1/Cx3cr1/p38 MAPK signaling axis}},
  author = {Xiang Zheng and Jiabao Dai and Changyuan Mao and Weidong Zhang and Jing Huang and Shuqin Hu},
  journal = {Frontiers in Pharmacology},
  year = {2026},
  month = oct,
  doi = {10.3389/fphar.2026.1953662},
  url = {https://www.frontiersin.org/articles/10.3389/fphar.2026.1953662/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Emodin attenuates CFA-induced inflammatory pain in association with suppression of the Cx3cl1/Cx3cr1/p38 MAPK signaling axis
AU  - Xiang Zheng
AU  - Jiabao Dai
AU  - Changyuan Mao
AU  - Weidong Zhang
AU  - Jing Huang
AU  - Shuqin Hu
PY  - 2026
DA  - 2026/10/14
JO  - Frontiers in Pharmacology
DO  - 10.3389/fphar.2026.1953662
UR  - https://www.frontiersin.org/articles/10.3389/fphar.2026.1953662/full
AB  - Objectives: To investigate the analgesic effect of emodin on Complete Freund’s Adjuvant (CFA)-induced inflammatory pain and to clarify the underlying molecular mechanism.  Methods: Emodin was administered intraperitoneally or prophylactically to attenuate CFA-induced inflammatory pain. RNA-seq was performed to identify the biological functions of differentially expressed genes in mouse dorsal root ganglion (DRG) tissues. The expression levels of Cx3cl1/Cx3cr1 were evaluated by RT-qPCR, Western blotting, and immunofluorescence. Pharmacological and genetic approaches were employed to block Cx3cr1 and assess its effect on pain thresholds in CFA-treated mice. Hematoxylin and eosin (H&E) staining was used to examine the infiltration of immune and inflammatory cells in dorsal root ganglion (DRG) tissues before and after emodin treatment. Following emodin treatment, the levels of p-p38/p38 in DRG tissues were determined by Western blotting, and the mRNA levels of the pro-inflammatory cytokines Tnf-α , Il-1β , and Il-6 in DRG tissues were measured by RT-qPCR.  Results: Both therapeutic and prophylactic administration of emodin effectively alleviated CFA-induced mechanical and thermal hypersensitivity. Emodin treatment suppressed the CFA-induced upregulation of Cx3cl1/Cx3cr1 mRNA and protein levels in the DRG. Pharmacological and genetic blockade of Cx3cr1 effectively attenuated CFA-induced hyperalgesia. In addition, emodin markedly inhibited p-p38/p38 protein expression in the DRG of mice with CFA-induced inflammatory pain, reduced immune cell infiltration in DRG tissues, and downregulated the levels of the pro-inflammatory cytokines Tnf-α , Il-1β , and Il-6 .  Conclusion: Emodin attenuated CFA-induced inflammatory pain in mice, an effect associated with reduced Cx3cl1/Cx3cr1 signaling, decreased p38 MAPK activation, diminished immune-cell infiltration in the DRG, and lower expression of the proinflammatory cytokines Tnf-α , Il-1β , and Il-6 in DRG tissue.
SN  - 1663-9812
ER  -