摘要
目的 探讨电针(EA)干预过氧化物酶体增殖物激活受体-γ(PPAR-γ)通路改善神经根型颈椎病(CSR)疼痛的机制及与自噬的关系。方法 将大鼠分为假手术组(Sham组)、CSR组、电针组(EA组)、EA+GW9622(PPAR-γ拮抗剂)组、EA+吡格列酮组。干预10、20、30 d后,检测各组大鼠神经痛阈值,并采用苏木精-伊红(HE)染色观察脊髓组织神经元细胞受损情况,TUNEL检测细胞凋亡情况,酶联免疫吸附实验检测白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、前列腺素E2(PEG2)和β-内啡肽(β-EP)水平,蛋白免疫印迹检测自噬相关蛋白PPAR-γ、微管相关蛋白1轻链3Ⅱ型(LC3Ⅱ)、Beclin-1蛋白表达。结果 与Sham组相比,CSR组大鼠神经痛阈值、β-EP、PPAR-γ、LC3Ⅱ、Beclin-1表达水平降低,细胞凋亡率、IL-1β、IL-6、TNF-α以及PEG2水平增高;与CSR组相比,EA组、EA+GW9622组、EA+吡格列酮组大鼠神经痛阈值、β-EP、PPAR-γ、LC3Ⅱ、Beclin-1表达水平增加,细胞凋亡率、IL-1β、IL-6、TNF-α以及PEG2降低;EA+GW9622组大鼠神经痛阈值、β-EP、PPAR-γ、LC3Ⅱ、Beclin-1表达水平低于EA组,细胞凋亡率、IL-1β、IL-6、TNF-α以及PEG2高于EA组;EA+吡格列酮组大鼠神经痛阈值、β-EP、PPAR-γ、LC3Ⅱ、Beclin-1表达水平高于EA组,细胞凋亡率、IL-1β、IL-6、TNF-α以及PEG2低于EA组;上述组间差异均有统计学意义(P<0.05)。结论 EA通过激活PPAR-γ通路介导的自噬来抑制脊髓组织病理损伤和细胞凋亡,减轻脊髓神经炎症反应,改善CSR模型的疼痛症状。
Objective To investigate the mechanism of electroacupuncture(EA)intervention in the peroxisome proliferator-activated receptor-(PPAR-)pathway for improving pain in cervicalspondylotic radiculopathy(CSR)and its relationship with autophagy.Methods Rats were divided into sham-operated group(Sham group),CSR group,EA group,EA+GW9662(PPAR-antagonist)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 apoptosis,the enzyme-linked immunosorbent assay(ELISA)wasused to detect the levels of interleukin-1β(IL-1β),interleukin-6(IL-6),tumor necrosis factor-α(TNF-α),prostaglandin E2(PGE2)andβ-endorphin(β-EP),and the Western blot analysis was used to detect the expression of autophagy-related proteins such as PPAR-,microtubule-associated protein 1 light chain 3 type I(LC3 I),and Beclin-1.Results Compared with the Sham group,the CSR group showed decreased neuralgia thresholds,β-EP,PPAR-,LC3 II and Beclin-1 expression levels,as well as increased cell apoptosis rate and IL-1β,IL-6,TNF-αand PGE2 levels;compared with the CSR group,the EA group,EA+GW9662 group,and EA+pioglitazone group showed increased neuralgia thresholds,β-EP,PPAR-,LC3 II and Beclin-1 expression levels as well as decreased cell apoptosis rates and IL-1β,IL-6,TNF-αand PGE2 levels;the neuralgia thresholds,β-EP,PPAR-,LC3 II,and Beclin-1 expression levels in the EA+GW9662 group were lower than those in the EA group,while the cell apoptosis rate and IL-1β,IL-6,TNF-αand PGE2 levels were higher;in contrast,the neuralgia thresholds,β-EP,PPAR-,LC3 I 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-1β,IL-6,TNF-αand 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-pathway.
作者
乔元座
QIAO Yuanzuo(Department of Traditional Chinese Orthopedics,Xingtai Hospital of Traditional Chinese Medicine in Hebei Province,Xingtai,Hebei,054000)
出处
《实用临床医药杂志》
2025年第9期75-79,85,共6页
Journal of Clinical Medicine in Practice
基金
河北省重点研发计划项目(22023891652D)。
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
electroacupuncture
cervical spondylotic radiculopathy
peroxisome proliferatoractivated receptor-
autophagy
prostaglandin E2
neuralgia
spinal cord neuroinflammatory responses
microtubule-associated protein 1 light chain 3 type I
