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. Author manuscript; available in PMC: 2018 Mar 1.
Published in final edited form as: Eur J Pain. 2016 Sep 15;21(3):456–465. doi: 10.1002/ejp.939

Figure 2.

Figure 2

Analgesia mediated by EDPs and sEHI is blocked mu-opioid antagonism. The analgesia mediated by 1 mg/kg EDPs co-administered with low dose 1mg/kg t-TUCB was blocked by naloxone (1 mg/kg) a mu-opioid receptor antagonist. The sEH inhibitor t-TUCB blocks the degradation of multiple classes of EpFA in vivo and a single administration of 10 mg/kg dose effectively induced a CPP response indicating pain relief (One Way ANOVA, p≤0.001). In the CPP assay this is indicated by increased time (seconds, y axis) spent in the drug paired chamber. The efficacy of 10 mg/kg t-TUCB was also blocked by naloxone. There was no significant effect of the naloxone in control neuropathic mice. The diabetic mice were assessed for phenotypic allodynia indicating diabetic neuropathy in the von Frey assay prior to the CPP assay. The results depicted below the graph are the grams of force to elicit a hind paw withdrawal (von Frey (gr)) of pre-streptozocin baseline scores (Naïve) and post streptozocin painful baseline scores (Diabetic) prior to the start of treatment in the CPP assay.