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目的探索鞘内注射氯胺酮能否通过抑制小胶质细胞的活化而治疗神经病理性痛。方法利用大鼠脊神经结扎(spinal nerve ligation,SNL)神经病理性痛模型,并鞘内注射氯胺酮,应用von Frey行为测试观察对大鼠基础痛阈和SNL所诱导的神经病理性痛的影响;通过免疫组织化学法检测其对大鼠脊髓背角小胶质细胞活化的影响。结果鞘内注射氯胺酮能够降低SNL诱导的机械性痛觉增敏,但对正常大鼠的机械性基础痛阈没有显著影响。同时鞘内注射氯胺酮能抑制SNL所诱导的大鼠脊髓背角小胶质细胞的活化,结合荧光强度半定量检测,观察到鞘内注射氯胺酮可以降低SNL诱导的小胶质细胞活化特异性标记物OX-42的表达。结论氯胺酮治疗神经病理性痛的镇痛机理可能是通过抑制神经损伤后小胶质细胞的活化。
Objective To explore whether intrathecal ketamine can treat neuropathic pain by inhibiting microglial activation. Methods The neuropathic pain model was induced by spinal nerve ligation (SNL) in rats and intrathecally injected with ketamine. The von Frey behavioral test was used to observe the effect on the pain threshold and neuropathic pain induced by SNL in rats. Effect of Chemiluminescence on Activation of Microglia in Spinal Dorsal Horn of Rats. Results Intrathecal ketamine reduced SNL-induced mechanical hyperalgesia but had no significant effect on the mechanical basis pain threshold in normal rats. At the same time, intrathecal ketamine could inhibit SNL-induced activation of microglia in the spinal dorsal horn of rats, combined with semi-quantitative detection of fluorescence intensity, it was observed that intrathecal ketamine could reduce SNL-induced microglial activation specific markers OX-42 expression. Conclusion The analgesic mechanism of ketamine in treating neuropathic pain may be through inhibiting the activation of microglia after nerve injury.