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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: Glial interleukin-1β upregulates neuronal sodium channel 1.7 in trigeminal ganglion contributing to temporomandibular joint inflammatory hypernociception in rats

Fig. 2

Upregulation of Nav1.7 expression by IL-1β was dependent on COX-2/PGE2/EP2 in TG explants. a Dose-course of COX-2 mRNA expression in TG after treatment with IL-1β (0.1 to 10 ng/mL) for 24 h. b Dose-course of COX-2 protein expression in TG after treatment with IL-1β (0.1 to 10 ng/mL) for 24 h. c Time-course of COX-2 mRNA expression in TG after treatment with IL-1β (10 ng/mL). d Time-course of COX-2 protein expression in TG after treatment with IL-1β. (E) IL-1β-induced upregulation of Nav1.7 mRNA expression in TG was blocked by COX-2 selective inhibitor NS398. f IL-1β-induced upregulation of Nav1.7 protein expression in TG was blocked by COX-2 selective inhibitor NS398. g EP2 selective antagonist PF-04418948 blocked upregulation of Nav1.7 mRNA expression, but not COX-2 mRNA expression in TG after treatment with IL-1β. h EP2 selective antagonist PF-04418948 blocked upregulation of Nav1.7 protein expression, but not COX-2 protein expression in TG after treatment with IL-1β. Quantification of protein expressions were presented as fold change of the control group (lower panel). One-way ANOVA, *P < 0.05 versus the control group, #P < 0.05 versus IL-1β group; n = 3. NS398: COX-2 selective inhibitor; PF-04418948: EP2 selective antagonist

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