脊髓巨噬细胞集落刺激因子及其受体在复杂性局部疼痛综合征Ⅰ型病程中的变化

Expressions of Spinal Macrophage Colony Stimulating Factor and Its Receptor CSF-1R in the Development of Complicated Regional Pain Symptom Ⅰ

目的 研究以大鼠后肢缺血再灌注所模拟的复杂性局部疼痛综合征Ⅰ型（CRPSⅠ）在建模后神经病理性疼痛行为学变化和脊髓组织中巨噬细胞集落刺激因子（M-CSF）和其受体CSF-1R在脊髓中的分布和表达。方法采用大鼠后肢缺血再灌注方法建立CRPSⅠ模型,在再灌注后14d内每天连续观察缺血足底机械痛阈和热痛阈的变化。采用免疫荧光双标染色技术显示脊髓M-CSF和CSF-1R在小胶质细胞和星状胶质细胞上的分布,以及在再灌注后3d、7d和14dM-CSF和CSF-1R表达量的变化。结果 在缺血再灌注后1~14d,缺血足底的机械痛阈和热痛阈均较对照组降低（P〈0.05）;M-CSF由脊髓星状胶质细胞分泌,其特异性受体CSF-1R则主要分布在脊髓小胶质细胞上;在再灌注后7d和14d,缺血同侧脊髓M-CSF和CSF-1R的表达较对照组增加（P〈0.05）。结论CRPSⅠ模型在建模后14d内,缺血同侧机械痛阈和热痛阈降低,缺血同侧脊髓组织中星状胶质细胞分泌的MCSF和小胶质细胞上的CSF-1R含量增加。

Objective To study the changes of mechanical allodynia and temperature hyperalgesia, as well as the expression of the spinal macrophage colony stimulating factor （M-CSF） and its receptor CSF-1R during the development of complicated regional pain symptom I （CRPS I ）. Methods The animal model of CRPS I was established using prolonged ischemia-reperfusion injury of rodent left hindpaw. The mechanical aliodynia and temperature hyperalgesia of ipsilateral hindpaw were continuously measured for 14 d after reperfusion, and the expressions of spinal M-CSF and CSF-1R in ipsilateral spinal cord horn were measured with immunofluorescence technique on day 3, day 7 and day 14 after reperfusion. Results The thresholds of mechanical allodynia and temperature hyperalgesia of ipsilateral hindpaw were significantly decreased （P〈0. 05）. M-CSF was secreted by the astrocytes. CSF-1R was primarily distributed on the microglia. The immunofluorescence intensities of M-CSF and CSF-1R in ipsilateral spinal cord horn were significantly increased on day 7 and day 14 after reperfusion （P〈0.05）. Conclusion The ischemia-reperfusion injury simulated pain syndrome in CRPS I and increased the expressions of spinal M-CSF and CSF-1R.