电针治疗化疗诱导的周围神经病变疼痛的实验证据：一项系统评价和荟萃分析。
完整摘要 · 中文译文
本研究系统评价了电针（EA）治疗化疗诱导的周围神经病变（CIPN）疼痛模型动物实验的证据。采用PICOS框架进行系统评价和荟萃分析，以评估电针的行为学和分子学效应，并阐明其潜在机制和转化潜力。共纳入13项符合条件的研究，涉及235只动物。方法学质量评分为5至8分，平均6.5分。荟萃分析显示，电针显著提高了缩足阈值（PWT）、热痛缩足潜伏期（PWL）和神经传导速度（NCV），同时减轻了冷异常性疼痛。在分子水平上，电针显著降低了促炎和敏化标志物的表达，包括TNF-α、IL-1β、GFAP、TLR4、TRPA1和TRPV1，并增加了氧化应激调节因子Nrf2。针对高度异质性的PWT结局进行了敏感性分析、发表偏倚评估、亚组分析和荟萃回归。识别出显著的发表偏倚，这可能解释了所观察到的大部分异质性。针对TRPV1的敏感性分析提示该结果可能受到个别研究的不成比例影响，因此应谨慎解读。其余结局的异质性可能反映了动物模型、穴位选择、治疗时长和干预方案的差异。总体而言，电针在CIPN模型中表现出镇痛和神经保护作用，主要通过调节神经炎症 形成、氧化应激的减弱以及神经元敏化的降低。这些发现提供了系统的临床前证据，支持电针（EA）作为CIPN疼痛有前景的辅助疗法，并强调需要进行高质量临床试验以优化治疗方案并促进临床转化。
完整摘要 · 英文原文
This study systematically evaluated the evidence from animal experiments on electroacupuncture (EA) for chemotherapy-induced peripheral neuropathy (CIPN) pain models. A systematic review and meta-analysis was conducted using the PICOS framework to assess the behavioral and molecular effects of EA and clarify its underlying mechanisms and translational potential. Thirteen eligible studies involving 235 animals were included. Methodological quality scores ranged from 5 to 8, with a mean of 6.5. Meta-analysis showed that EA significantly increased the paw withdrawal threshold (PWT), thermal pain withdrawal latency (PWL), and nerve conduction velocity (NCV), while reducing cold allodynia. At the molecular level, EA significantly decreased the expression of pro-inflammatory and sensitization markers, including TNF-α, IL-1β, GFAP, TLR4, TRPA1, and TRPV1, and increased the oxidative stress regulator Nrf2. Sensitivity analysis, publication bias assessment, subgroup analysis, and meta-regression were performed for the highly heterogeneous PWT outcome. Significant publication bias was identified and may account for much of the observed heterogeneity. Sensitivity analysis for TRPV1 suggested that this result may be disproportionately influenced by individual studies and should therefore be interpreted cautiously. Heterogeneity in the remaining outcomes likely reflects differences in animal models, acupoint selection, treatment duration, and intervention protocols. Overall, EA demonstrated analgesic and neuroprotective effects in CIPN models, primarily through modulation of neuroinflammation, attenuation of oxidative stress, and reduction of neuronal sensitization. These findings provide systematic preclinical evidence supporting EA as a promising adjuvant therapy for CIPN pain and highlight the need for high-quality clinical trials to optimize treatment protocols and facilitate clinical translation.