Fig. 2.

CXCR5 mediated EA analgesic effects by modulating neuron activity-related receptors, and neuropeptides. A–F EA alleviated the exacerbation of pain sensitivity induced by overexpression of CXCR5, and shRNA treatment increased the mechanical and thermal pain thresholds. Mean ± SEM. Two-way ANOVA, *p < 0.05, **  < 0.01, ***p < 0.001 vs. IS group, and #p < 0.05, ##p < 0.01, ###p < 0.001 vs. IS + AAV-Cxcr5 group. N = 12. Western blotting images and analysis showing the expression of CXCR5 G and CXCL13 H increased in Sp5C after overexpressing CXCR5, and silencing CXCR5 gene reduced their increased levels. Mean ± SEM. One-way ANOVA, (H)R² = 0.9148, (H)R² = 0.9457. I ELISA analysis showed that AAV-Cxcr5 increased expression of NR2B, SP and PACAP, and CXCR5-shRNA decreased the expression of them, like the effect of EA. Mean ± SEM. One-way ANOVA. EA: electroacupuncture; IS: inflammatory soup