NMDAR

Procaine pretreatment inhibits JAK2 and STAT3 expression. (A) Relative Jak2 mRNA level detected by qRT-PCR. (B) Relative Stat3 mRNA level detected by qRT-PCR. (C) JAK2 and STAT3 protein expression detected by western blot. (D) Relative protein levels of JAK2 and STAT3 based on Western blot results. sham, rats undergone sham surgery. CCI, rats undergone sciatic nerve chronic compression injury (CCI) as the neuropathic pain (NPP) model. CCI+procaine, NPP model rats pretreated with procaine. The detection is performed on the 20th day post surgery (n=3). GAPDH is used as an internal reference. *p<0.05, **p<0.01. JAK2, Janus kinase 2. STAT3, signal transducer and activator of transcription 3.

The NMDA receptor is involved in the neuroprotective effect of Res. MK 801 (2 mg/kg) was injected respectively at 30 min prior to cerebral ischemia or at 30 min prior to the administration of Res at 1 or 24 h pre-MCAO. (A) The effects of MK801 on ischemia-induced neuronal death when Res was administrated at 1 h pre-MCAO. (B) The effects of MK801 on ischemia-induced neuronal death when Res was administrated at 24 h pre-MCAO. n = 5 rats at each group.

(B) Vehicle-treated rats, BDNF-treated rats, rats pre-treated with CTX-B and rats pre-treated with Ifenprodil showed equivalenttime in the pairing chambers prior to the conditioning day. There were no differences in these groups;thus,the preconditioning values were pooled for graphical representation. Only BDNF-treated rats showed a clear preference for the chamber paired with spinal clonidine (10 g). *P < 0.05, compared with pre-conditioning, two-way ANOVA, F(1,1,1/20) = (23.25, 16.89, 10.97), n = 6/group. (C) Difference score, indicates that application of BDNF in intact rats increased the time spent in the clonidine-paired chamber, while pre-injection of CTX-B or Ifenprodil into the rACC attenuated the difference score. #P < 0.05, one-way ANOVA, F(3,20) = 15.38, n = 6/group. Data are expressed as the mean ± SEM.

Procaine pretreatment inhibits JAK2 and STAT3 expression. (A) Relative Jak2 mRNA level detected by qRT-PCR. (B) Relative Stat3 mRNA level detected by qRT-PCR. (C) JAK2 and STAT3 protein expression detected by western blot. (D) Relative protein levels of JAK2 and STAT3 based on Western blot results. sham, rats undergone sham surgery. CCI, rats undergone sciatic nerve chronic compression injury (CCI) as the neuropathic pain (NPP) model. CCI+procaine, NPP model rats pretreated with procaine. The detection is performed on the 20th day post surgery (n=3). GAPDH is used as an internal reference. *p<0.05, **p<0.01. JAK2, Janus kinase 2. STAT3, signal transducer and activator of transcription 3.

The NMDA receptor is involved in the neuroprotective effect of Res. MK 801 (2 mg/kg) was injected respectively at 30 min prior to cerebral ischemia or at 30 min prior to the administration of Res at 1 or 24 h pre-MCAO. (A) The effects of MK801 on ischemia-induced neuronal death when Res was administrated at 1 h pre-MCAO. (B) The effects of MK801 on ischemia-induced neuronal death when Res was administrated at 24 h pre-MCAO. n = 5 rats at each group.

(B) Vehicle-treated rats, BDNF-treated rats, rats pre-treated with CTX-B and rats pre-treated with Ifenprodil showed equivalenttime in the pairing chambers prior to the conditioning day. There were no differences in these groups;thus,the preconditioning values were pooled for graphical representation. Only BDNF-treated rats showed a clear preference for the chamber paired with spinal clonidine (10 g). *P < 0.05, compared with pre-conditioning, two-way ANOVA, F(1,1,1/20) = (23.25, 16.89, 10.97), n = 6/group. (C) Difference score, indicates that application of BDNF in intact rats increased the time spent in the clonidine-paired chamber, while pre-injection of CTX-B or Ifenprodil into the rACC attenuated the difference score. #P < 0.05, one-way ANOVA, F(3,20) = 15.38, n = 6/group. Data are expressed as the mean ± SEM.