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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: IL-33/ST2 signaling contributes to radicular pain by modulating MAPK and NF-κB activation and inflammatory mediator expression in the spinal cord in rat models of noncompressive lumber disk herniation

Fig. 5

Spinally delivered lentiviral vector LV-shIL-33 alleviates mechanical allodynia and decreases the production of spinal IL-1β, TNF-α, and COX-2, but not IL-6 in rat models of noncompressive lumbar disk herniation. a Paw withdrawal threshold was performed 1 day before the operation (baseline (BL)) and at different times (1, 3, 5, 7, 9, 11, 13, 15, 17, 19, and 21 days) after the operation. The values are the mean ± SEM (##p < 0.01 versus sham; **p < 0.01 versus the LV-NC group or the vehicle group, n = 10 in each group). b The expression levels of spinal COX-2 were assessed at the protein level by Western blotting 12 days after the operation. β-tubulin was used as the loading control. The results are expressed as the ratio of COX-2 to β-tubulin, and the control was set at 1.0. (c, d, and e). The expression levels of spinal IL-1β (c), IL-6 (d), and TNF-α (e) were assessed at the protein level by ELISA in each treatment group 12 days after the operation. The values are the mean ± SEM (##p < 0.01 versus sham; *p < 0.05 and **p < 0.01 versus the LV-NC group, n = 5–6 in each group)

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