Objective To observe the effect of electroacupuncture(EA)on the expression of high mobility group box 1(HMGB 1)and its receptor CD 24 proteins andβ-endorphin(β-EP)content in"Zusanli"(ST 36)region in rats with chronic constriction injury(CCI)

so as to explore its mechanisms underlying pain relief.Methods Thirty male Wistar rats were randomized into control

CCI model and EA groups(n=10 rats in each).The neuropathic pain model was established by ligature of the left sciatic nerve to induce CCI in the model and EA groups

and sham operation was performed in rats of the control group.Paw with drawal latency(PWL

thermal pain threshold)of the bilateral hind-limbs was detected by using an algesia-detector.Eight days after CCI operation

EA was applied to bilateral"Zusanli"(ST 36)and"Yanglingquan"(GB 34)for 30 min

once daily for5 days.The acetylated-HMGB 1 expression was determined by immunoprecipitation

and the expression of HMGB 1 and toll like receptor 4(TLR 4)proteins and CD 24 mRNA were detected using Western blot and fluorescent quantitative real time-PCR

respectively

and the content ofβ-EP in the acupoint region was assayed by enzyme linked immunosorbent assay(ELISA).AntiCD 24 neutralizing antibody(200 !L

100!g/mL)was injected into ST 36 region once daily for 3 days for verifying the involvement of HMGB 1/CD 24 signaling in EA analgesia.Results Compared with the control group

the bilateral PWL difference values in the other two groups were significantly increased(P<0.05)

meaning an occurrence of hyperalgesia after CCI.In comparison with the CCI model group

the hyperalgesia in the EA group was obviously decreased(P<0.05).After CCI

the expression levels of HMGB 1 and TLR 4 proteins were considerably increased compared with those in the control group(P<0.05).After 5-times' EA

the acetylated-HMGB 1

the expression of CD 24 mRNA

and the content ofβ-EP were notably up-regulated(P<0.05)

and there were no obvious changes in the expression levels of HMGB 1 and TLR 4 proteins(P>0.05).After local injection of anti-CD 24 antibody

EA-induced increases ofβ-EP content and reduction of thermal pain threshold were significantly suppressed(P<0.05).Conclusion EA of ST 36 and GB 34 can alleviate neuropathic pain in CCI rats

which is associated with its effects in up-regulatingβ-EP content

and HMGB 1 protein and CD 24 mRNA expression levels in ST 36 region.The activated HMGB 1/CD 24/β-EP signaling contributes to EA-ST 36 induced analgesia.