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Fig. 5. Graphs illustrating the effect of DHEAS on the development of neuropathic pain originally inhibited by i.t. administration of L-NIL in CCI rats. (A and B) Paw withdrawal frequency (PWF, %) was measured in the hind paw using a von-Frey filament (2.0 g). Intrathecal (i.t.) co-administration of dehydroepiandrosterone sulfate (DHEAS; 3 or 10 nmol) with L-NIL (60 nmol) restored the PWF (A) and the area under curve (AUC, %) data (B) that were inhibited by administration of L-NIL (60 nmol) alone. (C and D) Paw withdrawal latency (PWL, s) was measured in the hind paw using a plantar analgesia meter. Co-administration of DHEAS (3 or 10 nmol) with L-NIL (60 nmol) restored the PWL (C) and the AUC (%) data (D) that were originally inhibited by administration of L-NIL (60 nmol) alone. Drugs or vehicle were administrated twice a day from days 0 to 5 post-surgery. n=6 rats/ group. *p<0.05, **p<0.01, ***p<0.001 vs. L-NIL-treated group. A and C, two-way ANOVA followed by a Bonferroni multiple comparison test for post-hoc analysis. B and D, one-way ANOVA followed by a Newman-Keuls multiple comparison test for post-hoc analysis.
Exp Neurobiol. 2019;28:516~528 https://doi.org/10.5607/en.2019.28.4.516
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