目的 探讨养帕方对亚急性帕金森病模型小鼠行为学和疼痛症状的治疗效果及其可能的作用机制。方法 共42只无特定病原体级C57BL/6J小鼠随机分为对照组，模型组，养帕方低剂量组[13.50 g/（kg·d）]、中剂量组[40.50 g/（kg·d）]和高剂量组[121.50 g/（kg·d）]，多巴丝肼组（每组各7只）。采用爬杆实验、悬挂实验和旷场实验评估小鼠行为学改变，热痛反应潜伏期测量仪和电子压力测痛仪测量热刺激伤害性感受阈和机械刺激伤害性感受阈，免疫组化染色检测黑质和杏仁核酪氨酸羟化酶（TH）阳性表达量。结果 不同处理组小鼠爬杆时间（F=14.625,P=0.000）、悬挂评分（F=24.493,P=0.000）和静止时间（F=24.506,P=0.000），热刺激伤害性感受阈值（F=24.726,P=0.000）和机械刺激伤害性感受阈值（F=21.052,P=0.000），黑质（F=19.663,P=0.000）和杏仁核（F=36.513,P=0.000）TH阳性表达量差异均具有统计学意义。与对照组相比，模型组爬杆时间（P=0.000）和静止时间（P=0.000）延长，悬挂评分（P=0.000）、热刺激伤害性感受阈值（P=0.000）和机械刺激伤害性感受阈值（P=0.000）、黑质（P=0.000）和杏仁核（P=0.000）TH阳性表达量降低。与模型组相比，养帕方低剂量组、中剂量组、高剂量组和多巴丝肼组爬杆时间（P=0.020,0.000,0.000,0.000）和静止时间（P=0.000,0.000,0.000,0.000）缩短，但仍长于对照组（均P <0.05）；悬挂评分（P=0.000,0.000,0.000,0.000）、热刺激伤害性感受阈值（P=0.008,0.000,0.000,0.000）和机械刺激伤害性感受阈值（P=0.003,0.000,0.000,0.000）、黑质（P=0.031,0.001,0.000,0.000）和杏仁核（P=0.007,0.000,0.000,0.000）TH阳性表达量增加，除多巴丝肼组热刺激伤害性感受阈值恢复至对照组水平（P=0.063）外，其余3组仍低于对照组（均P <0.05）。与养帕方低剂量组比较，养帕方中剂量组、高剂量组和多巴丝肼组爬杆时间（P=0.009,0.009,0.006）和静止时间（P=0.024,0.018,0.001）亦缩短，但仍长于对照组（均P <0.05）；悬挂评分（P=0.015,0.011,0.002）、热刺激伤害性感受阈值（P=0.001,0.001,0.000）和机械刺激伤害性感受阈值（P=0.035,0.001,0.001）、黑质（P=0.043,0.023,0.001）和杏仁核（P=0.007,0.005,0.000）TH阳性表达量亦增加，除多巴丝肼组杏仁核TH阳性表达量高于养帕方中剂量组（P=0.009）和高剂量组（P=0.012）外，养帕方中剂量组、高剂量组和多巴丝肼组各项指标差异无统计学意义（均P> 0.05）。结论 养帕方可以有效改善亚急性帕金森病模型小鼠行为学和疼痛症状，推测是通过保护黑质和杏仁核多巴胺能神经元实现的。