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电针可减轻持续性炎症大鼠的行为性痛觉过敏,并选择性降低其脊髓Fos蛋白表达。

Electro-acupuncture attenuates behavioral hyperalgesia and selectively reduces spinal Fos protein expression in rats with persistent inflammation.

作者信息

Lao L, Zhang G, Wei F, Berman B M, Ren K

机构信息

Complementary Medicine Program, University of Maryland School of Medicine, Baltimore, 21207, USA.

出版信息

J Pain. 2001 Apr;2(2):111-7. doi: 10.1054/jpai.2001.19575.

Abstract

This study examined the effect of electro-acupuncture (EA) on persistent inflammatory hyperalgesia in a rat model. Inflammation and hyperalgesia were induced by injecting complete Freund's adjuvant (CFA) into one hindpaw of the rat. Hyperalgesia was determined by a decrease in paw withdrawal latencies (PWL) to a noxious thermal stimulus. EA was applied bilaterally at the acupuncture point Huantiao (G30) at the rat's hindlimbs. EA-treated rats (n = 11) had significantly longer PWLs as compared with placebo control rats (n = 7) in the inflamed paw at 2.5 hours and 5 days after injection of CFA (P <.05) and longer PWLs as compared to sham control rats (n = 9) at 2.5 hours (P >.05). Paw edema was significantly reduced in EA-treated rats versus placebo controls at 24 hours after inflammation (P <.01). Inflammation-induced spinal Fos expression in the medial half of laminae I-II in EA-treated rats versus placebo rats (n = 5 per group) was significantly reduced (P <.01). These data showed that EA delayed the onset and facilitated the recovery of inflammatory hyperalgesia and suppressed the inflammation-induced spinal Fos expression in neurons (laminae I-II) involved in receiving noxious stimulation. This rat model of persistent pain and inflammation seems to be an ideal animal model for studying the effect of acupuncture.

摘要

本研究在大鼠模型中考察了电针(EA)对持续性炎性痛觉过敏的影响。通过向大鼠一侧后爪注射完全弗氏佐剂(CFA)诱导炎症和痛觉过敏。通过对有害热刺激的缩爪潜伏期(PWL)缩短来确定痛觉过敏。在大鼠后肢环跳穴(G30)双侧施加电针。与安慰剂对照大鼠(n = 7)相比,电针治疗的大鼠(n = 11)在注射CFA后2.5小时和5天时,患侧爪子的PWL显著延长(P <.05);与假手术对照大鼠(n = 9)相比,在2.5小时时PWL也延长(P >.05)。与安慰剂对照组相比,电针治疗的大鼠在炎症后24小时时爪部水肿显著减轻(P <.01)。与安慰剂大鼠(每组n = 5)相比,电针治疗的大鼠炎症诱导的脊髓I-II层内侧半层Fos表达显著降低(P <.01)。这些数据表明,电针延迟了炎性痛觉过敏的发作并促进其恢复,抑制了参与接收有害刺激的神经元(I-II层)中炎症诱导的脊髓Fos表达。这种持续性疼痛和炎症的大鼠模型似乎是研究针刺作用的理想动物模型。

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