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. Author manuscript; available in PMC: 2015 Mar 15.
Published in final edited form as: Eur J Pharmacol. 2014 Jan 28;727:87–98. doi: 10.1016/j.ejphar.2014.01.026

Fig.3.

Fig.3

Summary data of effects of araC treatment (10μg/animal for 7 days; i.t.) on VMR to CRD in naïve rats and TNBS-treated rats. (A) While TNBS-treated rats exhibited significant visceral hyperalgesia (shown in blue; data extrapolated from Fig. 1C), rats treated with araC for 7 days post-TNBS administration into the colon failed to develop visceral hyperalgesia, observed with no significant (P<0.05) change in their VMR (shown in red). (B) In naïve, non-inflamed rats, araC treatment for 7 days did not cause any significant alteration in the VMRs and were comparable to the baseline values. Values expressed as mean ± S.E.M. of ‘n’ animals in each study group. (C) Iba-1 positive stained sections of LS spinal cord from araC + TNBS-treated rat. Scale bar represent 200μm. (DI) GFAP-ir sections from S1 DRG of araC + TNBS-treated rats. Scale bar represent 50μm. (E) The number of activated microglial was significantly decreased in araC + TNBS-treated rats compared to TNBS-treated rats (TNBS data reused from Fig. 2B for comparison). Values are expressed as mean % of activated cells ± S.E.M. (F) The mean grey intensity from GFAP-ir sections from both L6 and S1 DRGs was found to be significantly (P<0.05) decreased when compared to TNBS-treated rats (TNBS data reused from Fig. 2C for comparison). Values expressed as mean grey intensity of GFAP ± S.E.M. P<0.05 was considered significant. * compared with TNBS-treated rats.