目的 探讨阿咖酚散对疱疹病毒后遗神经痛模型大鼠的镇痛作用，并研究其可能的作用机制。方法 通过大鼠胫骨神经注射人疱疹病毒1型诱导神经痛模型。造模成功后，将大鼠随机分为对照组、模型组、普瑞巴林组（27 mg/kg）、阿咖酚散（52、105、210 mg/kg）组。通过测定机械缩足阈值及热板舔足次数评估痛行为学变化。酶联免疫吸附测法检测大鼠血清中白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）、P物质（SP）水平；HE染色检测脊髓组织病理学变化；采用实时荧光定量PCR法检测神经痛模型大鼠脊髓组织中Janus激酶2（JAK2）、信号转导和转录激活因子3（STAT3）、降钙素基因相关肽（CGRP）、巨噬细胞趋化蛋白-1（MCP-1）mRNA表达水平。结果 与模型组比较，给药第3天，阿咖酚散52、210 mg/kg组痛阈值显著升高；给药第5天，阿咖酚散各剂量组痛阈值显著上升（P＜0.05、0.01）。与模型组比较，给药第3天，阿咖酚散各剂量组大鼠舔足次数显著减少；给药第5天，阿咖酚散210 mg/kg组大鼠舔足次数显著减少（P＜0.05、0.01）。与模型组相比，阿咖酚散105、210 mg/kg组动物脊髓病理评分显著下降（P＜0.05、0.01）。与模型组比较，阿咖酚散各剂量组大鼠血清TNF-α水平显著降低，阿咖酚散105、210 mg/kg组大鼠血清SP水平显著降低（P＜0.05、0.01）。与模型组比较，阿咖酚散各剂量组CGRP、MCP1 mRNA表达显著降低，阿咖酚散105、210 mg/kg组STAT3 mRNA表达显著降低（P＜0.05、0.01）。结论 阿咖酚散对疱疹后神经痛模型大鼠具有明确的镇痛作用，其机制可能与下调疼痛相关基因表达，抑制神经系统的局部炎症反应和神经损伤，从而干预神经敏化过程有关。

Objective To investigate the analgesic effect of the Paracetamol, Caffeine and Aspirin Powder on rat models of postherpetic neuralgia, and to explore its potential mechanisms of action. Method The rat sciatic nerve was injected with human herpesvirus type 1 to establish a model of neuropathic pain. After successful modeling, the rats were randomly divided into the control group, the model control group, the pregabalin group (27 mg/kg), and Paracetamol, Caffeine and Aspirin Powder (52, 105, 210 mg/kg) groups. The changes in pain behavior were evaluated by measuring the mechanical withdrawal threshold and the number of paw licking on the hot plate. The levels of IL-6, TNF-α, and SP in the rat serum were detected by enzyme-linked immunosorbent assay. The pathological changes of the spinal cord tissue were detected by HE staining, and the mRNA expression levels of JAK2, STAT3, CGRP, and MCP-1 in the spinal cord tissue of the neuropathic pain model rats were detected by real-time fluorescence quantitative PCR. Result Compared with the model group, on the 3rd day after administration, the pain threshold in the Paracetamol, Caffeine and Aspirin Powder (52 and 210 mg/kg) groups was significantly increased, on the 5th day after administration, the pain threshold in all dose groups of Paracetamol, Caffeine and Aspirin Powder was significantly increased (P < 0.05, 0.01). Compared with the model group, on the 3rd day after administration, the number of paw licking in all dose groups of Paracetamol, Caffeine and Aspirin Powder in rats was significantly reduced, on the 5th day after administration, the number of paw licking in the Paracetamol, Caffeine and Aspirin Powder 210 mg/kg group in rats was significantly reduced (P < 0.05, 0.01).Compared with the model group, the spinal cord pathological scores of the animals in the Paracetamol, Caffeine and Aspirin Powder (105 and 210 mg/kg) significantly decreased (P< 0.05, 0.01). Compared with the model group, the serum TNF-α levels of the rats in each dose group of Paracetamol, Caffeine and Aspirin Powder significantly decreased, and the serum SP levels of the rats in the Paracetamol, Caffeine and Aspirin Powder 105 and 210 mg/kg groups were significantly decreased (P < 0.05, 0.01). Compared with the model group, the mRNA expressions of CGRP and MCP1 in each dose group of Paracetamol, Caffeine and Aspirin Powder were significantly decreased, and the STAT3 mRNA expression in the Paracetamol, Caffeine and Aspirin Powder 105 and 210 mg/kg groups were significantly decreased (P < 0.05, 0.01). Conclusion Paracetamol, Caffeine and Aspirin Powder has a definite analgesic effect on rats with herpes-induced post-neuralgia pain. The mechanism may be related to the down-regulation of pain-related gene expression, inhibition of local inflammatory responses and nerve damage in the nervous system, thereby interfering with the process of nerve sensitization.

R971