Gua Sha Alleviates Radiculitis-Induced Pain Via HIF-1α-Mediated Metabolic Reprogramming Pathway in Rats.

IF 2.5 3区 医学 Q2 CLINICAL NEUROLOGY
Pain Research & Management Pub Date : 2025-03-17 eCollection Date: 2025-01-01 DOI:10.1155/prm/9923147
Haotian Ge, Shuxia Yan, Mingwan Yin, Yujie Gao, Jiayi Wang, Qin Wang, Guihua Xu, Min Yang
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引用次数: 0

Abstract

Background: Radiculitis-induced pain (RIP) results from dorsal root ganglion (DRG) sensitization due to inflammation. Hypoxia-inducible factor 1-alpha (HIF-1α) is linked to inflammatory responses through metabolic changes, but its role in RIP is not well understood. Gua Sha therapy has been shown to reduce inflammation and neural damage from lumbar disc herniation (LDH). This study investigates whether HIF-1α-mediated metabolic reprogramming contributes to the pain-relieving effects of Gua Sha in RIP. Methods: Male SD rats were subjected to LDH surgery and divided into six groups: sham, model, sham Gua Sha, Gua Sha, Gua Sha + DMOG, and Gua Sha + YC-1. Gua Sha was applied 5 days postsurgery, every other day for three sessions per course, totaling three courses. Changes in paw withdrawal threshold (PWT) and latency (PWL) were monitored, along with blood flow in the rats' backs. Levels of IL-1β, TNF-α, and NF-κB were assessed in serum and DRG tissue. Pathological changes and hypoxia in DRG tissues were observed using hematoxylin-eosin staining and immunofluorescence. Western blotting and qPCR measured HIF-1α, GLUT1, PFKM, and PDK1 expression, while lactic acid and ATP levels in DRG tissue were also evaluated. Results: Gua Sha increased PWT and PWL, reduced serum and DRG inflammatory factors, improved back microcirculation, alleviated DRG hypoxia, and decreased HIF-1α and related signaling factors. It also lowered lactic acid and raised ATP levels. DMOG, a HIF-1α activator, reversed these effects. HIF-1α activation did not affect serum inflammatory factors but partially improved PWT. Inhibition of HIF-1α with YC-1 did not significantly differ from Gua Sha alone. Conclusion: HIF-1α-mediated metabolic reprogramming is a pathogenic mechanism in RIP. Gua Sha alleviates RIP by enhancing microcirculation, improving DRG hypoxia, inhibiting HIF-1α-mediated reprogramming, and reducing DRG sensitization and inflammation. This study provides insights into the mechanisms of Gua Sha's therapeutic effects in RIP.

刮痧通过HIF-1α介导的代谢重编程途径缓解大鼠根管炎引起的疼痛
背景:神经根炎引起的疼痛(RIP)是由炎症引起的背根神经节(DRG)致敏引起的。缺氧诱导因子1- α (HIF-1α)通过代谢变化与炎症反应有关,但其在RIP中的作用尚不清楚。瓜沙疗法已被证明可以减少腰椎间盘突出症(LDH)的炎症和神经损伤。本研究探讨hif -1α介导的代谢重编程是否参与瓜沙在RIP中的镇痛作用。方法:雄性SD大鼠行LDH手术,分为假、模型、假瓜沙、瓜沙、瓜沙+ DMOG、瓜沙+ YC-1 6组。瓜沙于术后第5天应用,每隔一天一次,每疗程3次,共3个疗程。监测足爪戒断阈值(PWT)和潜伏期(PWL)的变化,以及大鼠背部的血流量。检测血清及DRG组织中IL-1β、TNF-α、NF-κB水平。采用苏木精-伊红染色和免疫荧光法观察DRG组织的病理变化和缺氧情况。Western blotting和qPCR检测HIF-1α、GLUT1、PFKM和PDK1的表达,同时评估DRG组织中乳酸和ATP的水平。结果:瓜沙增加PWT和PWL,降低血清和DRG炎症因子,改善背部微循环,减轻DRG缺氧,降低HIF-1α及相关信号因子。它还能降低乳酸,提高ATP水平。HIF-1α激活剂DMOG逆转了这些效应。HIF-1α激活不影响血清炎症因子,但部分改善PWT。YC-1对HIF-1α的抑制作用与单独番薯无显著差异。结论:hif -1α介导的代谢重编程是RIP发病机制之一。番沙可通过增强微循环、改善DRG缺氧、抑制hif -1α介导的重编程、减轻DRG致敏和炎症来缓解RIP。本研究为瓜沙治疗RIP的作用机制提供了新的思路。
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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来源期刊
Pain Research & Management
Pain Research & Management CLINICAL NEUROLOGY-
CiteScore
5.30
自引率
0.00%
发文量
109
审稿时长
>12 weeks
期刊介绍: Pain Research and Management is a peer-reviewed, Open Access journal that publishes original research articles, review articles, and clinical studies in all areas of pain management. The most recent Impact Factor for Pain Research and Management is 1.685 according to the 2015 Journal Citation Reports released by Thomson Reuters in 2016.
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