ABSTRACT
Objective To evaluate the effect of intrathecal oxytocin on neuropathic pain in rats.Methods Thirty-six SPF male Sprague-Dawley rats,aged 4-6 weeks,weighing 100-150 g,were divided into 4 groups (n =9 each) using a random number table:control group (group C),neuropathic pain group (group NP),neuropathic pain plus normal saline group (group NPN) and neuropathic pain plus oxytocin group (group NPO).The neuropathic pain model was made by partial sciatic nerve injury in NP,NPN and NPO groups.In group NPO,oxytocin l0 μl (0.1 μg) was intrathecally injected on the day of establishing the model and 1 and 2 days after establishing the model,and then normal saline 10 μl was given for tube sealing at 9 a.m.and 4 p.m.every day.In group NPN,normal saline 20 μl was given for tube sealing at the corresponding time points.The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured at 1 day before establishing the model and 1,2,3,4,5,6 and 7 days after establishing the model.The expression of the astrocyte marker glial fibrillary acidic protein (GFAP) and a specific marker of microglia ionized calcium-binding adaptor molecule 1 (IBa-1) was detected by Western blot at 1 day before establishing the model and 3 and 7 days after establishing the model.Results Compared with group C,the MWT was significantly decreased,TWL was shortened and the expression of GFAP and IBa-1 was up-regulated at each time point in NP and NPN groups (P＜0.05).There was no significant difference in MWT,TWL GFAP and IBa-1 at each time point between group NPN and group NP (P＞0.05).Compared with NP group,MWT was significantly increased at 2-4 days after establishing the model,TWL was prolonged at 1-4 days after establishing the model,the expression of IBa-1 was down-regulated on 3 days after establishing the model,and the expression of GFAP was downregulated on 3 and 7 days after establishing the model in group NPO (P＜0.05).Conclusion Oxytocin can reduce neuropathic pain,and the mechanism may be related to inhibiting activation of glial cells in the spinal cord of rats.