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电针对 CFA 诱导的大鼠炎性疼痛脊髓 p38MAPK/ATF-2/VR-1 通路的干预作用。

Intervention of electroacupuncture on spinal p38 MAPK/ATF-2/VR-1 pathway in treating inflammatory pain induced by CFA in rats.

机构信息

Department of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, 548 Binwen Road, Binjiang District, Hangzhou, Zhejiang Province 310053, China.

出版信息

Mol Pain. 2013 Mar 22;9:13. doi: 10.1186/1744-8069-9-13.

DOI:10.1186/1744-8069-9-13
PMID:23517865
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3608238/
Abstract

BACKGROUND

Previous studies have demonstrated that p38 MAPK signal transduction pathway plays an important role in the development and maintenance of inflammatory pain. Electroacupuncture (EA) can suppress the inflammatory pain. However, the relationship between EA effect and p38 MAPK signal transduction pathway in inflammatory pain remains poorly understood. It is our hypothesis that p38 MAPK/ATF-2/VR-1 and/or p38 MAPK/ATF-2/COX-2 signal transduction pathway should be activated by inflammatory pain in CFA-injected model. Meanwhile, EA may inhibit the activation of p38 MAPK signal transduction pathway. The present study aims to investigate that anti-inflammatory and analgesic effect of EA and its intervention on the p38 MAPK signal transduction pathway in a rat model of inflammatory pain.

RESULTS

EA had a pronounced anti-inflammatory and analgesic effect on CFA-induced chronic inflammatory pain in rats. EA could quickly raise CFA-rat's paw withdrawal thresholds (PWTs) and maintain good and long analgesic effect, while it subdued the ankle swelling of CFA rats only at postinjection day 14. EA could down-regulate the protein expressions of p-p38 MAPK and p-ATF-2, reduced the numbers of p-p38 MAPK-IR cells and p-ATF-2-IR cells in spinal dorsal horn in CFA rats, inhibited the expressions of both protein and mRNA of VR-1, but had no effect on the COX-2 mRNA expression.

CONCLUSIONS

The present study indicates that inhibiting the activation of spinal p38 MAPK/ATF-2/VR-1 pathway may be one of the main mechanisms via central signal transduction pathway in the process of anti-inflammatory pain by EA in CFA rats.

摘要

背景

先前的研究表明，p38MAPK 信号转导通路在炎症性疼痛的发生和维持中起着重要作用。电针（EA）可以抑制炎症性疼痛。然而，EA 效应与炎症性疼痛中的 p38MAPK 信号转导通路之间的关系尚不清楚。我们假设，在 CFA 注射模型中，炎症痛会激活 p38MAPK/ATF-2/VR-1 和/或 p38MAPK/ATF-2/COX-2 信号转导通路。同时，EA 可能会抑制 p38MAPK 信号转导通路的激活。本研究旨在探讨 EA 在炎症性疼痛大鼠模型中的抗炎镇痛作用及其对 p38MAPK 信号转导通路的干预作用。

结果

EA 对 CFA 诱导的慢性炎症性疼痛大鼠具有明显的抗炎和镇痛作用。EA 可迅速提高 CFA 大鼠的足潜伏期（PWT），并保持良好且持久的镇痛效果，而对 CFA 大鼠的踝关节肿胀仅在注射后第 14 天起作用。EA 可下调 p-p38MAPK 和 p-ATF-2 的蛋白表达，减少 CFA 大鼠脊髓背角中 p-p38MAPK-IR 细胞和 p-ATF-2-IR 细胞的数量，抑制 VR-1 的蛋白和 mRNA 表达，但对 COX-2 mRNA 表达无影响。

结论

本研究表明，抑制脊髓 p38MAPK/ATF-2/VR-1 通路的激活可能是 EA 通过中枢信号转导通路在 CFA 大鼠抗炎痛过程中的主要机制之一。

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