Fang Jian-Qiao, Fang Jun-Fan, Liang Yi, Du Jun-Ying, Qiu Yu-Jie, Liu Jin
The Third Clinical Medical College, Zhejiang University of CM, Hangzhou 310053, China.
Zhongguo Zhen Jiu. 2012 Nov;32(11):1007-11.
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.
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.
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).
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.
观察电针（EA）对弗氏完全佐剂（CFA）诱导的急性炎性疼痛大鼠脊髓背角（SCDH）细胞外信号调节激酶1/2（ERK1/2）磷酸化的影响，进一步从细胞信号转导方面阐明EA即时镇痛的机制。
将53只健康雄性SD大鼠分为两批。第一批23只大鼠采用CFA建立炎性疼痛模型，观察大鼠 paw withdrawal thresholds（PWTs）的变化，并用免疫组化法检测患侧SCDH中p-ERK1/2阳性细胞。第二批30只大鼠随机分为空白对照组（N组）、CFA组和EA组，每组10只。CFA组和EA组大鼠采用CFA诱导炎性疼痛，EA组于造模后5.5 h给予EA治疗，观察PWTs及SCDH中p-ERK1/2阳性细胞的变化。
第一批大鼠在给予CFA后5 h、3 d、7 d和14 d时PWTs明显降低（均P<0.01）。然而，患侧SCDH中p-ERK1/2阳性细胞仅在注射CFA后5 h增加，造模后3 d恢复正常。第二批实验中，与N组同一时间点相比，CFA组和EA组大鼠造模后PWTs均明显降低（均P<0.01）。EA组大鼠接受一次EA治疗后的PWTs长于EA治疗前及CFA组同一时间点相应的PWTs（均P<0.01）。此外，造模后6 h，CFA组患侧SCDH中p-ERK1/2阳性细胞数量显著增加（P<0.01），而EA组则显著减少（P<0.01）。
抑制SCDH的ERK1/2激活可能是EA产生即时镇痛效应的细胞信号转导关键机制之一。
