Fig. 5
From: Capsazepine decreases corneal pain syndrome in severe dry eye disease
Evaluation of the expression of genes involved in pain conduction and the modulation of pain responses in the TG of untreated sham and DED animals and DED animals treated with 10 μM capsazepine or vehicle on d21. RT-qPCR analysis of ipsilateral TG of sham mice, DED mice, and DED mice treated with 10μM capsazepine or vehicle: glial-inflammatory cell communication genes (a), inhibition of targets related to nociceptive inhibition (b), intracellular signal transduction genes (c), voltage-gated ion channel genes (d), synaptic transmission genes (e), inflammation genes (f). Total number of mice = 19. Number of mice included in the analysis = 19. Sham mice, DED mice, and DED ice-treated with 10μM capsazepine or vehicle: n =4–5. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 relative to sham animals. $ < 0.05: DED treated with vehicle relative to DED. £ < 0.05, ££ < 0.01, £££ < 0.001: DED treated with capsazepine relative to DED, # P<0.05: DED treated with capsazepine relative to DED treated with vehicle. Results are expressed as the mean ± SEM. For statistical analysis, the Kolmogorov–Smirnov test was performed followed by a nonparametric Mann-Whitney test or a parametric t-test using GraphPad Prism version 7.00 (GraphPad Software, La Jolla, CA, USA)