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Fig. 2. Graphs illustrating the effect of i.t. administration of the NOS-II inhibitor, L-NIL on the development of neuropathic pain in CCI rats. (A and B) Paw withdrawal frequency (PWF, %) was measured in the hind paw using a von-Frey filament (2.0 g). Sciatic nerve injury increased PWF, and this increase was dose-dependently suppressed by intrathecal (i.t.) administration of L-NIL (A; 6, 20 or 60 nmol). The area under curve (AUC, %) data analysis showed an analgesic effect of L-NIL on CCI-induced mechanical allodynia (B). (C and D) Paw withdrawal latency (PWL, s) was measured in the hind paw using a plantar analgesia meter. Sciatic nerve injury decreased PWL, and this decrease was dose-dependently suppressed by i.t. administration of L-NIL (B; 6, 20 or 60 nmol). The AUC (%) data analysis showed an analgesic effect of L-NIL on CCI-induced thermal hyperalgesia (D). Drug or vehicle was administrated twice a day from days 0 to 5 post-surgery. n=6 rats/group. ***p<0.001 vs. Sham; #p<0.05, ##p<0.01, ###p<0.001 vs. vehicle-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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