Low-Frequency Electroacupuncture Alleviates Chronic Constrictive Injury-Induced Mechanical Allodynia

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Objective:To study the effects of electroacupuncture (EA) in chronic constrictive injury (CCI) rat model and the expression of N-methyl-D-aspartate receptor type 2B (NR2B) in ipsilateral spinal dorsal horn in rats to explore the analgesic mechanisms of EA.Methods:According to the random number table,totally 180 rats were evenly divided into a sham group,a CCI group,and an EA group.CCI model was conducted with four 4-0 chromic gut ligatures loosely ligated around the left sciatic nerve 1 cm above the trifurcation.Rats in the EA group received 2 Hz EA therapy bilaterally at acupoints of Zusanli (ST 36) and Sanyinjiao (SP 6) once daily (30 min/d) for 30 days after surgery.Paw withdrawal thresholds (PWTs) were measured on 0 (baseline),1,3,7,15,30 days after surgery.Rats were sacrificed on 0,1,3,7,15 and 30 days after surgery,and the L4-5 segments of spinal cord were removed to detect the expression of NR2B by immunohistochemistry and quantitative polymerase chain reaction.Results:PWTs in the CCI group were significantly lower than the sham group at Day 1-30 after surgery,and reached its lowest at Day 1 (P<0.01).After EA treatment,the PWTs recovered rapidly and were significantly higher than those in the CCI group on 3,7,15 and 30 days after surgery (P<0.01).The numbers of NR2B-immunoreactive cells of the CCI group significantly increased after CCI surgery compared with the sham group (P<0.01).Compared with the CCI group,stimulation of EA markedly decreased the numbers of NR2B-immunoreactive cells at Day 3,7,15 and 30 (P<0.05).In the sham group,NR2B mRNA was expressed at a low level.It increased after CCI surgery,which increased rapidly at Day 7 (P<0.01) and reached its peak value at Day 15 (P<0.01).After EA stimulation,relative quantity of NR2B mRNA expression was less than that in the CCI group at Day 15 and 30 (P<0.05).Conclusions:Low frequency of EA had antinociceptive effect in CCI rat model.The analgesic effects of EA might be through the inhibition of NR2B.
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