电针对佐剂性关节炎大鼠下丘脑和脊髓腺苷A_1受体表达的影响

Effect of Electroacupuncture on the Expression of Adenosine A1 Receptor in Hypothalamus and Spinal Cord of Adjuvant Arthritis Rats

目的观察腺苷A1受体对疼痛及电针镇痛的影响,探讨电针镇痛的作用机制。方法以佐剂性关节炎大鼠为研究对象,将24只大鼠随机分为正常组、模型组和电针组,每组8只。应用辐射热行为测痛法观察佐剂性关节炎大鼠的痛阈变化,采用免疫组化法、实时荧光定量PCR法观察腺苷A1受体在下丘脑和脊髓的表达及电针的影响。结果造模后1 d,模型组和电针组右后足痛阈与同组造模前比较,差异均具有统计学意义(P<0.01)。模型组和电针组造模后1 d右后足痛阈与正常组比较,差异均具有统计学意义(P<0.01)。造模后7 d,模型组大鼠右后足痛阈仍明显低于同组造模前(P<0.01),与正常组和电针组比较,差异均具有统计学意义(P<0.01)。电针组大鼠造模后7 d痛阈提高,与同组造模后1 d比较,差异具有统计学意义(P<0.01)。模型组阳性细胞表达降低,与正常组比较,差异具有统计学意义(P<0.01)。电针组较模型组ADORA1表达增强,两组比较差异具有统计学意义(P<0.01)。模型组下丘脑和脊髓的ADORA1m RNA表达下调,与正常组比较,差异均具有统计学意义(P<0.01)。电针组下丘脑和脊髓组织的ADORA1m RNA表达上调,与模型组比较,差异均具有统计学意义(P<0.01)。结论电针能够上调佐剂性关节炎大鼠下丘脑和脊髓腺苷A1受体的表达。

Objective To observe the effect of adenosine A1 receptor on pain and electroacupuncture analgesia, and to explore the action mechanism of electroacupuncture in analgesia. Method Adjuvant arthritis rats were taken as the study subjects. 24 rats were randomized into a normal group, a model group and an electroacupuncture（EA） group, 8 rats in each group. The pain threshold was evaluated by using thermal radiation method, immunohistochemical method and real-time fluorescence quantitative PCR were adopted to observe the expression of adenosine A1 receptor in hypothalamus and spinal cord. Result One day after modeling, the pain thresholds of right hind paw in the model group and EA group were significantly changed compared to that before modeling in the same group（P〈0.01）. The pain thresholds of right hind paw in the model group and EA group were significantly different from that in the normal group one day after modeling（P〈0.01）. 7 d after modeling, the pain threshold of right hind paw in the model group was still significantly lower than that before modeling in the same group（P〈0.01）, and it was significantly different from that in the normal group and EA group（P〈0.01）. The pain threshold was significantly enhanced in the EA group 7 d after modeling, and was significantly different from that of 1 d after modeling in the same group（P〈0.01）. The positive cell expression was lower in the model group and was significantly different from that in the normal group（P〈0.01）. The expression of adenosine A1 receptor in the EA group was markedly higher than that in the model group（P〈0.01）. The expression of adenosine A1 receptor in hypothalamus and spinal cord of the model group was significantly lower than that of the normal group（P〈0.01）. The expression of adenosine A1 receptor in hypothalamus and spinal cord of EA group was markedly higher than that of the model group（P〈0.01）. Conclusion EA can up-regulate the expression of adenosine A1 receptor in hypothalamus and spinal cord of adjuvant arthritis rats.