title: [Immediate analgesic effect of electroacupuncture and its regulation mechanism via spinal p-ERK1/2].
abstract: OBJECTIVE
  To observe influence of electroacupuncture (EA) on phosphorylation of extracellular signal-regulated kinases 1/2 (ERK1/2) in spinal cord dorsal horn (SCDH) in rats with acute inflammatory pain induced by complete Freund's adjuvant (CFA), further elucidate the immediate analgesic mechanism of EA via cellular signal transduction.
  
  
  METHODS
  Fifty-three healthy male SD rats were divided into two batches. The inflammatory pain models of the first batch of 23 rats were established by using CFA. The changes of the paw withdrawal thresholds (PWTs) of rats were observed and positive cells of p-ERK1/2 in affected SCDH were detected by using immunohistochemistry method. The second batch of 30 rats were randomly divided into a blank control group (N group), CFA group and EA group, 10 rats in each group. The rats of CFA group and EA group were induced inflammatory pain by using CFA, and the EA group was treated with EA at 5.5 h after the model establishment. The changes of PWTs and the positive cells of p-ERK1/2 in SCDH were observed.
  
  
  RESULTS
  The PWTs of the first batch of rats obviously decreased at 5 h, 3 d, 7 d and 14 d after CFA administration (all P< 0.01). However, the p-ERK1/2 positive cells in affected SCDH only increased at 5 h after CFA-injection and returned to normality at 3 d after the model establishment. In the second batch, compared with that of N group at the same time point, PWTs of rats in both CFA and EA group obviously decreased after the model establishment (both P<0.01). PWTs of rats in EA group which accepted EA treatment once were longer than those before EA treatment and corresponding PWTs in CFA group at the same time point (both P<0.01). Moreover, the numbers of p-ERK1/2 positive cells of affected SCDH increased significantly in CFA group at 6 h after the model establishment (P<0.01), however, which were decreased significantly in EA group (P<0.01).
  
  
  CONCLUSIONS
  Inhibiting ERK1/2 activation of SCDH may be one of the pivotal mechanism of cellular signal transduction of the immediate analgesic effect educed by EA.
authors.affiliation: The Third Clinical Medical College, Zhejiang University of CM, Hangzhou 310053, China. fangjianqiao7532@163.com
authors.forename: Jian-Qiao
authors.initials: JQ
authors.lastname: Fang
authors.forename: Jun-Fan
authors.initials: JF
authors.lastname: Fang
authors.forename: Yi
authors.initials: Y
authors.lastname: Liang
authors.forename: Jun-Ying
authors.initials: JY
authors.lastname: Du
authors.forename: Yu-Jie
authors.initials: YJ
authors.lastname: Qiu
authors.forename: Jin
authors.initials: J
authors.lastname: Liu
mesh_terms: D015667:Acupuncture Analgesia; D000818:Animals; D001416:Back Pain / Q000139:chemically induced / Q000201:enzymology / Q000235:genetics / Q000628:therapy*; D015671:Electroacupuncture; D005620:Freund's Adjuvant / Q000009:adverse effects; D006801:Humans; D008297:Male; D019950:Mitogen-Activated Protein Kinase 1 / Q000235:genetics / Q000378:metabolism*; D048052:Mitogen-Activated Protein Kinase 3 / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013131:Spine / Q000201:enzymology*
chemical_list: D005620:Freund's Adjuvant; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3