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电针对完全弗氏佐剂注射大鼠谷氨酸转运体下调的抑制作用产生抗伤害作用。

Electroacupuncture Confers Antinociceptive Effects via Inhibition of Glutamate Transporter Downregulation in Complete Freund's Adjuvant-Injected Rats.

机构信息

Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University, Gyeongnam 626-870, Republic of Korea.

出版信息

Evid Based Complement Alternat Med. 2012;2012:643973. doi: 10.1155/2012/643973. Epub 2012 Aug 23.

DOI:10.1155/2012/643973
PMID:22956975
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3432559/
Abstract

When we evaluated changes of glial fibrillary acidic protein (GFAP) and two glutamate transporter (GTs) by immunohistochemistry, expression of GFAP showed a significant increase in complete Freund's adjuvant (CFA)-injected rats; however, this expression was strongly inhibited by electroacupuncture (EA) stimulation. Robust downregulation of glutamate-aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1) was observed in CFA-injected rats; however, EA stimulation resulted in recovery of this expression. Double-labeling staining showed co-localization of a large proportion of GLAST or GLT-1 with GFAP. Using Western blot, we confirmed protein expression of two GTs, but no differences in the mRNA content of these GTs were observed. Because EA treatment resulted in strong inhibition of CFA-induced proteasome activities, we examined the question of whether thermal sensitivities and GTs expression could be regulated by proteasome inhibitor MG132. CFA-injected rats co-treated with EA and MG132 showed a significantly longer thermal sensitivity, compared with CFA-injected rats with or without MG132. Both EA and MG132 blocked CFA-induced GLAST and GLT-1 downregulation within the spinal cord. These results provide evidence for involvement of GLAST and GLT-1 in response to activation of spinal astrocytes in an EA antinociceptive effect. Antinociceptive effect of EA may be induced via proteasome-mediated regulation of spinal GTs.

摘要

当我们通过免疫组织化学评估胶质纤维酸性蛋白 (GFAP) 和两种谷氨酸转运体 (GTs) 的变化时，发现完全弗氏佐剂 (CFA) 注射大鼠的 GFAP 表达显著增加；然而，电针 (EA) 刺激强烈抑制了这种表达。CFA 注射大鼠中观察到谷氨酸-天冬氨酸转运体 (GLAST) 和谷氨酸转运体-1 (GLT-1) 的强烈下调；然而，EA 刺激导致了这种表达的恢复。双标记染色显示大量 GLAST 或 GLT-1 与 GFAP 共定位。通过 Western blot，我们证实了两种 GTs 的蛋白表达，但这些 GTs 的 mRNA 含量没有差异。由于 EA 处理导致 CFA 诱导的蛋白酶体活性强烈抑制，我们研究了热敏感性和 GTs 表达是否可以通过蛋白酶体抑制剂 MG132 调节的问题。与未用 MG132 处理的 CFA 注射大鼠相比，同时接受 EA 和 MG132 处理的 CFA 注射大鼠的热敏感性明显延长。EA 和 MG132 均阻断了脊髓中 CFA 诱导的 GLAST 和 GLT-1 下调。这些结果为 GLAST 和 GLT-1 参与 EA 镇痛效应中脊髓星形胶质细胞的激活提供了证据。EA 的镇痛作用可能是通过蛋白酶体介导的脊髓 GTs 调节诱导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d9/3432559/4a4846ad9b3d/ECAM2012-643973.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d9/3432559/6f7c57635e47/ECAM2012-643973.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d9/3432559/f172b919e986/ECAM2012-643973.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d9/3432559/4a4846ad9b3d/ECAM2012-643973.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d9/3432559/6f7c57635e47/ECAM2012-643973.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d9/3432559/c7cc8d547595/ECAM2012-643973.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d9/3432559/2b193ee8f466/ECAM2012-643973.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d9/3432559/e5ce516663a1/ECAM2012-643973.004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d9/3432559/f172b919e986/ECAM2012-643973.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d9/3432559/4a4846ad9b3d/ECAM2012-643973.007.jpg

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