Electroacupuncture alleviates the transition from acute to chronic pain through the p38 MAPK/TNF-α signalling pathway in the spinal dorsal horn.

Ying Jin, Jie Zhou, Fangfang Xu, Zeqin Ren, Jun Hu, Cong Zhang, Kaiwen Ge, Lanying Liu
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引用次数: 6

Abstract

Background: Hyperalgesic priming (HP) is a model of the transition from acute to chronic pain. Electroacupuncture (EA) could inhibit pain development through the peripheral dorsal root ganglia; however, it is unclear whether it can mitigate the transition from acute to chronic pain by attenuating protein expression in the p38 MAPK (mitogen-activated protein kinase)/tumour necrosis factor alpha (TNF-α) pathway in the spinal dorsal horn.

Aims: We aimed to determine whether EA could prevent the transition from acute to chronic pain by affecting the p38 MAPK/TNF-α pathway in the spinal dorsal horn in a rat model established using HP.

Methods: We first randomly subdivided 30 male Sprague-Dawley (SD) rats into 5 groups (n = 6 per group): control (N), sham HP (Sham-HP), HP, HP + SB203580p38 MAPK (HP+SB203580), and HP + Lenalidomide (CC-5013) (HP+Lenalidomide). We then randomly subdivided a further 30 male SD rats into 5 groups (n = 6 per group): Sham-HP, HP, sham EA (Sham EA), EA (EA), and EA + U-46619 p38 MAPK agonist (EA+U-46619). We assessed the effects of EA on the mechanical paw withdrawal threshold and p38 MAPK/TNF-α expression in the spinal dorsal horn of rats subjected to chronic inflammatory pain.

Results: Rats in the EA group had reduced p38 MAPK and TNF-α expression and had significantly reduced mechanical hyperalgesia compared with rats in the other groups.

Conclusion: Our findings indicate that EA could increase the mechanical pain threshold in rats and inhibit the transition from acute pain to chronic pain. This mechanism could involve reduced p38 MAPK/TNF-α expression in the spinal dorsal horn.

电针通过脊髓背角p38 MAPK/TNF-α信号通路缓解急性到慢性疼痛的转变。
背景:痛觉过敏启动(Hyperalgesic priming, HP)是急性疼痛向慢性疼痛过渡的一个模型。电针可通过外周背根神经节抑制疼痛的发展;然而,尚不清楚它是否可以通过降低脊髓背角中p38 MAPK(丝裂原活化蛋白激酶)/肿瘤坏死因子α (TNF-α)通路的蛋白表达来减轻从急性到慢性疼痛的转变。目的:我们的目的是确定EA是否可以通过影响HP建立的大鼠脊髓背角p38 MAPK/TNF-α通路来阻止从急性到慢性疼痛的转变。方法:首先将30只雄性SD大鼠随机分为5组(每组n = 6):对照组(n)、假HP (sham -HP)、HP、HP+ SB203580p38 MAPK (HP+SB203580)、HP+来那度胺(CC-5013) (HP+来那度胺)。然后,我们将30只雄性SD大鼠随机分为5组(每组n = 6):假HP、HP、假EA (sham EA)、EA (EA)和EA+U-46619 p38 MAPK激动剂(EA+U-46619)。我们评估了EA对慢性炎症性疼痛大鼠机械足退出阈值和脊髓背角p38 MAPK/TNF-α表达的影响。结果:与其他各组相比,EA组大鼠p38 MAPK和TNF-α表达降低,机械性痛觉过敏明显减轻。结论:EA可提高大鼠机械痛阈值,抑制急性痛向慢性痛的转变。这一机制可能与脊髓背角p38 MAPK/TNF-α表达降低有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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