脊髓CXCR2在CCI大鼠神經(jīng)病理性疼痛中的作用研究
發(fā)布時間:2018-04-17 10:12
本文選題:神經(jīng)病理性疼痛 + 趨化因子受體; 參考:《中國現(xiàn)代醫(yī)學(xué)雜志》2017年14期
【摘要】:目的 探討脊髓趨化因子受體2(CXCR2)在坐骨神經(jīng)慢性壓迫(CCI)模型大鼠神經(jīng)病理性疼痛(NPP)中的作用。方法 18只成年Sprague-Dawley雄性大鼠,隨機分為3組,每組6只。對照組:大鼠不做任何處理;模型組:復(fù)制CCI大鼠模型;實驗組:復(fù)制CCI大鼠模型后第3天腹腔注射漆樹酸5 mg/kg。于復(fù)制大鼠CCI模型前1天,以及第1、3、5和7天分別測定大鼠后足熱痛閾及機械痛閾,并應(yīng)用Western blot測定腰段脊髓CXCR2的蛋白表達。結(jié)果 CCI大鼠術(shù)后第3天開始術(shù)側(cè)下肢熱痛閾值降低,模型組、實驗組術(shù)側(cè)下肢熱痛閾值與對照組比較,差異有統(tǒng)計學(xué)意義(P0.05);實驗組大鼠第5和7天術(shù)側(cè)熱痛閾值與模型組比較,差異有統(tǒng)計學(xué)意義(P0.05)。機械痛閾變化趨勢與熱痛閾一致。模型組、實驗組大鼠脊髓CXCR2表達與對照組比較,差異有統(tǒng)計學(xué)意義(P0.05);實驗組CXCR2表達與模型組比較,差異有統(tǒng)計學(xué)意義(P0.05)。結(jié)論 脊髓CXCR2表達的異常上調(diào),可導(dǎo)致NPP產(chǎn)生和維持。腹腔注射漆樹酸能夠部分抑制CCI大鼠脊髓腰段CXCR2的表達上調(diào),并緩解CCI大鼠的疼痛行為。
[Abstract]:Objective to investigate the role of CXCR2 in neuropathic pain induced by chronic compression of sciatic nerve in rats.Methods 18 adult Sprague-Dawley male rats were randomly divided into 3 groups with 6 rats in each group.Control group: rats did not do any treatment; model group: CCI rat model; experimental group: 3 days after CCI rat model was intraperitoneally injected with 5 mg 路kg ~ (-1) of lactoic acid.The heat pain threshold and mechanical pain threshold of the hind foot were measured one day before the CCI model was established, and the expression of CXCR2 protein in the lumbar spinal cord was measured by Western blot.Results the lower extremity thermal pain threshold of the CCI rats was decreased from the 3rd day after operation. The thermal pain threshold of the model group and the experimental group was compared with that of the control group.There was significant difference between the experimental group and the model group on the 5th and 7th day, the difference was statistically significant (P 0.05).The change trend of mechanical pain threshold is consistent with thermal pain threshold.In the model group, the expression of CXCR2 in the spinal cord of the experimental group was significantly higher than that in the control group (P 0.05), while the expression of CXCR2 in the experimental group was significantly higher than that in the model group (P 0.05).Conclusion the abnormal upregulation of CXCR2 expression in spinal cord may lead to the production and maintenance of NPP.Intraperitoneal injection of lactoxylic acid partially inhibited the up-regulation of CXCR2 expression in spinal cord of CCI rats and alleviated the pain behavior of CCI rats.
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