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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: NFATc2-dependent epigenetic upregulation of CXCL14 is involved in the development of neuropathic pain induced by paclitaxel

Fig. 1

The upregulation of NFATc2 in dorsal horn neurons was involved in the mechanical allodynia induced by paclitaxel. a Treatment with paclitaxel decreased the hind paw withdraw threshold in rats (**P < 0.01 vs the vehicle group/day 10, n = 12 per group). b Representative blots and histogram showed the upregulation of NFATc2 following paclitaxel application on both total and nucleus level (**P < 0.01 vs the vehicle group/day 10, n = 4 per group). c The immunofluorescence signal of NFATc2 (red) was colocalized with NeuN (neurons marker, green), but not Iba-1 (microglia marker, green) or GFAP (astrocyte marker, green) or Sox10 (oligodendrocyte maker, green) in both vehicle group and paclitaxel group. Left scale bar, 100 μm; right scale bar, 20 μm (n = 3 per group). d, e Intrathecal injection of the NFATc2 siRNA significantly decreased the expression of NFATc2 mRNA and protein (**P < 0.01 vs the scramble group, n = 5 or 4 per group). f, g Deletion of NFATc2 in dorsal horn significantly attenuated the mechanical allodynia and thermal hyperalgesia induced by paclitaxel in the rats (**P < 0.01 vs the vehicle group, ##P < 0.01 vs the paclitaxel group, n = 12 per group)

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