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. Author manuscript; available in PMC: 2023 Apr 7.
Published in final edited form as: J Pain. 2022 Nov 20;24(4):605–616. doi: 10.1016/j.jpain.2022.11.006

Figure 1.

Figure 1.

Local C781 decreases PAR2-mediated mechanical hypersensitivity and grimacing when coinjected with 2AT, a PAR2-specific agonist, and blocks hyperalgesic priming. Baseline (BL) measures were obtained before male and female C57BL6 mice received an intraplantar hind paw coinjection of 20.9 ng PAR2 agonist, 2AT, along with 1 μg of PAR2 antagonist, C781. When compared to mice that received only 2AT, mice that received C781 showed decreased (A) acute mechanical sensitivity and (B) facial grimacing. Mice that received only C781 intraplantar injection showed no mechanical hypersensitivity nor grimacing, indicating that local C781 does not cause pain on its own. To assess for hyperalgesic priming, mice were allowed to return to baseline levels and then injected with 100 ng of PGE2 into the hind paw. (C and D) Mice that received C781 cotreatment showed decreased 2AT-induced hyperalgesic priming revealed by the loss of PGE2 response. For the 2AT + Vehicle group, n = 2 females and n = 3 males. For the 2AT + C781 group, n = 3 females and n = 3 males. For the Vehicle + C781 group, n = 2 females and n = 3 males. *P < .05, **P < .01, ***P < .001, ****P < .0001. For paw withdrawal threshold and grimace scores, repeated measures two-way ANOVA with Dunnett post-test was used. All group mean comparisons were made to the mean of the 2AT + Vehicle group.