坐骨神经慢性压榨性损伤大鼠的热痛敏与淋巴细胞参与的免疫机制有关

慢性神经病理性疼痛通过常规镇痛治疗难以好转。目前有观点认为淋巴细胞相关的免疫机制可能参与该疾病发生发展的环节。为了初步验证这个观点,本实验通过手术制作大鼠坐骨神经慢性压榨性损伤(CCI)模型,在此基础上,从术后3d起每日给予环孢素A(CsA)抑制淋巴细胞增殖。结果显示:在术后13d,与NS模型组比较,CsA组大鼠外周血液淋巴细胞总数下降到40%左右,脾小体萎缩,动脉周围淋巴鞘有核细胞减少;同时热刺激引起患肢回缩所需的时间延长。以上结果提示淋巴细胞相关的免疫机制参与了CCI大鼠热痛敏的调节;这一结论为寻找新的治疗方案提供了线索。

The thermal hyperalgesia in rats with chronic constriction injury of sciatic nerve is related to the lymphocyte-involved mechanism

Traditional methods of analgesia can not ease the chronic neuropathic pain.There is an opinion recently that lymphocyte-involved mechanisms may control the initiation or sustaining of chronic pain.In order to supply some evidence for this opinion,we made the rat model of chronic constriction injury(CCI),and then injected cyclosporine A(CsA) since the 3rd day post operation to inhibit the proliferation of lymphocytes.The results showed that at the 13th day post operation,the total number of lymphocytes in CsA group was deceased to approximately 40% compared to the NS group,and the lymphoid nodules and periarterial lymphatic sheaths were atrophied,too.At the same time,the hind paw reduced thermal latencies of operated side went up.These results suggest that lymphocyte-involved mechanisms may modulate the thermal hyperalgesia in CCI rats,and provide a clue for the searching of new therapeutic strategies.