| 摘要: | 本研究的目的在於：一、探討電針是否能抑制小鼠後頸皮下注射致癢劑引起的強烈搔癢行為包括； (1) 5’-guanidinonaltrindole (GNTI)是一種由化學合成的致癢藥物，為κ類鴉片受器拮抗劑。 (2) 血清素；為一種發炎調控因子及 (3) 化合物48/80; 一種常見可快速引起皮膚及結締組織肥大細胞釋放組織胺的化合物。二、以免疫組織化學染色法(immunohistochemistry method)檢視電針是否能抑制小鼠皮下注射致癢劑引起脊髓背角外側神經元的c-fos蛋白表現。
結果發現於小鼠合谷(LI4)及曲池(LI11)施以2 Hz電針對GNTI (0.3 mg/kg 及 0.6 mg/kg)能抑制其引起的搔癢行為，100 Hz則沒有作用；100 Hz電針對化合物48/80 (10 mg/kg)引起的搔癢有抑制作用，但2 Hz電針則沒有作用；而2 Hz和100 Hz電針皆可抑制血清素(100 nmol/site)引起的搔癢行為。另以 [d-Ala2,N-Me-Phe4, Gly5-ol]-enkephalin acetate (DAMGO；μ類鴉片受體作用劑)及trans-(1S,2S)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)cyclohexyl] benzeneacetamide hydrochloride hydrate (U50488H；κ類鴉片受體作用劑，探討低頻及高頻電針之機轉，發現血清素及GNTI引起的搔癢行為可被DAMGO及 U50488H抑制；而化合物48/80引起的搔癢行為只能被U50488H抑制。
GNTI及化合物48/80於頸椎脊髓背角外側引起c-fos表現，於合谷(LI4)及曲池(LI11)施以2 Hz電針有效抑制GNTI引起的c-fos表現；100 Hz電針有效抑制化合物48/80引起的c-fos表現。
本研究推論電針抑制GNTI、化合物48/80與血清素引起的搔癢行為與電針之頻率相關；而μ及κ類鴉片受體可能與電針之止癢的機轉相關。
The aims of the present study were as follows: (1) to investigate the influence of electroacupuncture (EA) on compulsive scratching in mice elicited by the subcutaneous administration behind the neck of the following pruritogens: (a) 5′-guanidinonaltrindole (GNTI), a κ opioid antagonist, (b) serotonin (5-HT), an inflammatory mediator, and (c) compound 48/80, a common pruritogen that rapidly releases inflammatory mediators such as histamine from mast cells in connective tissue and skin; and (2) to determine the effects of EA on suppressing c-fos expression provoked by subcutaneously injected pruritogens. We discovered that the application of EA to the LI4 and LI11 acupoints at 2 Hz, but not at 100 Hz, attenuated GNTI (0.3 mg/kg and 0.6 mg/kg; s.c.)-induced scratching. EA at 100 Hz, but not at 2 Hz, attenuated compound 48/80 (10 mg/kg)-induced scratching. EA at 2 and 100 Hz attenuated 5-HT (100 nmol/site)-induced scratching. Moreover, [D-Ala2, N-Me-Phe4, Gly5-ol]-enkephalin acetate (DAMGO) (10 nmol/site), a well-established selective μ-opioid receptor agonist, significantly reduced GNTI- and 5-HT-induced scratching behavior, but not that from compound 48/80, while trans-(1S,2S)-3,4-dichloro-N-methyl-N-[2- (1-pyrrolidinyl) cyclohexyl] benzeneacetamide hydrochloride hydrate (U-50488H) (10 nmol/site), a selective κ opioid receptor agonist, attenuated all pruritogen-induced mice scratching behavior. GNTI and compound 48/80 provoked c-fos expression on the lateral side of the superficial layer of the dorsal horn in the cervical spinal cord. The application of 2 Hz EA to LI4 and LI11 decreased the number of c-fos-positive nuclei induced by GNTI. In addition, the application of 100 Hz EA to LI4 and LI11 decreased the number of c-fos-positive nuclei induced by compound 48/80. It is concluded that EA attenuates the scratching behavior induced by GNTI, compound 48/80, and 5-HT in mice in a frequency-dependent manner. The μ and κ opioid systems are involved, at least in part, in the anti-pruritic effects of EA. |
