Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2016
[Expressions of Spinal Macrophage Colony Stimulating Factor and Its Receptor CSF-1R in the Development ofComplicated Regional Pain Symptom I].
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Liao Zhi-Min, Tang Yu-Ying, Zheng Yang-Chun, Xu Dan
Аннотация
OBJECTIVES: 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 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).
CONCLUSIONS: The ischemia-reperfusion injury simulated pain syndrome in CRPS I and increased the expressions of spinal M-CSF and CSF-1R.
METHODS: The animal model of CRPS I 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).
CONCLUSIONS: The ischemia-reperfusion injury simulated pain syndrome in CRPS I and increased the expressions of spinal M-CSF and CSF-1R.