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 ofComplicated Regional Pain Symptom Ⅰ

中文关键词:  复杂性局部疼痛综合征Ⅰ型 巨噬细胞集落刺激因子 小胶质细胞

英文关键词:Complicated regional pain symptom Ⅰ Macrophage colony stimulating factor Microglia

中文摘要:

      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14 d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3 d、7 d和14 d M-CSF和CSF-1R表达量的变化。结果 在缺血再灌注后1~14 d，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7 d和14 d，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14 d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M-CSF和小胶质细胞上的CSF-1R含量增加。

英文摘要:

      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 symptomⅠ(CRPSⅠ). Methods The animal model of CRPSⅠ was established using prolonged ischemia-reperfusion injury of rodent left hindpaw. The mechanical allodynia 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 CRPSⅠand increased the expressions of spinal M-CSF and CSF-1R.