实用临床医药杂志2025，Vol.29Issue(9)：75-79,85,6.DOI:10.7619/jcmp.20244922
电针干预过氧化物酶体增殖物激活受体-γ通路增加自噬改善神经根型颈椎病疼痛的模型研究
Model study on improvement of cervical spondylotic radiculopathy pain by increasing autophagy through electroacupuncture intervention in peroxisome proliferator-activated receptor-γ pathway
摘要
Abstract
Objective To investigate the mechanism of electroacupuncture(EA)intervention in the peroxisome proliferator-activated receptor-γ(PPAR-γ)pathway for improving pain in cervical-spondylotic radiculopathy(CSR)and its relationship with autophagy.Methods Rats were divided into sham-operated group(Sham group),CSR group,EA group,EA+GW9662(PPAR-γ antago-nist)group,and EA+pioglitazone group.After 10,20 and 30 days of intervention,the neuralgia threshold of the rats in each group was measured;the hematoxylin and eosin(HE)staining was used to observe the damage to neuronal cells in the spinal cord tissue,TUNEL was used to detect cell ap-optosis,the enzyme-linked immunosorbent assay(ELISA)wasused to detect the levels of interleukin-1β(IL-1 β),interleukin-6(IL-6),tumor necrosis factor-α(TNF-α),prostaglandin E2(PGE2)and β-endorphin(β-EP),and the Western blot analysis was used to detect the expression of autoph-agy-related proteins such as PPAR-γ,microtubule-associated protein 1 light chain 3 type Ⅱ(LC3Ⅱ),and Beclin-1.Results Compared with the Sham group,the CSR group showed decreased neu-ralgia thresholds,β-EP,PPAR-γ,LC3 Ⅱ and Beclin-1 expression levels,as well as increased cell apoptosis rate and IL-1 β,IL-6,TNF-α and PGE2 levels;compared with the CSR group,the EA group,EA+GW9662 group,and EA+pioglitazone group showed increased neuralgia thresholds,β-EP,PPAR-γ,LC3 Ⅱ and Beclin-1 expression levels as well as decreased cell apoptosis rates and IL-1 β,IL-6,TNF-α and PGE2 levels;the neuralgia thresholds,β-EP,PPAR-γ,LC3 Ⅱ,and Be-clin-1 expression levels in the EA+GW9662 group were lower than those in the EA group,while the cell apoptosis rate and IL-1 β,IL-6,TNF-α and PGE2 levels were higher;in contrast,the neu-ralgia thresholds,β-EP,PPAR-γ,LC3 Ⅱ and Beclin-1 expression levels in the EA+pioglitazone group were higher than those in the EA group,with lower cell apoptosis rates and IL-1 β,IL-6,TNF-α and PGE2 levels;the differences mentioned above were statistically significant between the different groups(P＜0.05).Conclusion EA inhibits pathological damage and cell apoptosis in spinal cord tissue,reduces spinal cord neuroinflammatory responses,and improves pain symptoms in CSR models by activating autophagy mediated by the PPAR-γ pathway.关键词
电针/神经根型颈椎病/过氧化物酶体增殖物激活受体-γ/自噬/前列腺素E2/神经痛/脊髓神经炎症反应/微管相关蛋白1轻链3Ⅱ型Key words
electroacupuncture/cervical spondylotic radiculopathy/peroxisome proliferator-activated receptor-γ/autophagy/prostaglandin E2/neuralgia/spinal cord neuroinflammatory re-sponses/microtubule-associated protein 1 light chain 3 type Ⅱ分类
医药卫生引用本文复制引用
乔元座..电针干预过氧化物酶体增殖物激活受体-γ通路增加自噬改善神经根型颈椎病疼痛的模型研究[J].实用临床医药杂志,2025,29(9):75-79,85,6.基金项目
河北省重点研发计划项目(22023891652D) （22023891652D）
