【摘要】 目的:探讨β-1,4-半乳糖基转移酶-I(β-1,4-galactosyltransferase-I,β-1,4-GalT-I)和肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)在腰椎关节突关节炎(lumbar facet arthritis,LFA)模型大鼠背根神经节(dorsal root ganglia,DRG)中的表达及其意义。方法:将成年SD大鼠随机分为对照组和实验组,实验组使用弗氏完全佐剂制作大鼠LFA模型。检测大鼠机械性缩足阈值的变化;运用蛋白质印迹检测大鼠DRG中β-1,4-GalT-I和TNF-α的表达和丝裂原活化蛋白激酶(mitogen activated protein kinase,MAPK)信号通路的激活情况;运用免疫荧光双标检测大鼠DRG中β-1,4-GalT-I和TNF-α的分布和共定位情况。结果:与对照组相比,实验组大鼠在第3、5和7天机械性缩足阈值明显降低;DRG中β-1,4-GalT-I和TNF-α蛋白水平在第3、5和7天升高并在第5天达到峰值,然后逐渐恢复到正常水平。β-1,4-GalT-I和TNF-α在DRG神经元细胞和神经胶质细胞中均有表达,而且在第5天时,β-1,4-GalT-I和TNF-α在实验组大鼠DRG神经元细胞和神经胶质细胞中的表达均较对照组明显增加;实验组大鼠DRG中β-1,4-GalT-I和TNF-α存在共定位和MAPK信号通路激活。结论:大鼠LFA炎症可以导致DRG中神经元细胞和神经胶质细胞β-1,4-GalT-I和TNF-α表达增加,可能与LFA引起的下肢神经症状密切相关。更多还原

【Abstract】 Objective: To explore the expression and significance of β-1,4-galactosyltransferase-I (β-1,4-GalT-I) and tumor necrosis factor-α (TNF-α) in dorsal root ganglia(DRG) of rat lumbar facet arthritis(LFA) model.Methods: Adult SD rats were randomly divided into control group and experimental group. For the experimental group, Freund′s complete adjuvant was used to make rat LFA model.Mechanical withdrawal threshold was used to test the change of the mechanical thresholds of the rat foot.The expression of β-1,4-GalT-I and TNF-α in rat DRG and the activation of mitogen activated protein kinase(MAPK) signaling pathway were detected by Western blotting. The distribution and co-localization of β-1,4-GalT-I and TNF-α in DRG of rats were detected by immunofluorescence double labeling.Results: Compared with the control group, the mechanical thresholds of the foot of rats in the experimental group on the 3 rd, 5 th and 7 th days were significantly lower; β-1,4-GalT-I and TNF-α protein levels increased on the 3 rd, 5 th and 7 th days and reached a peak on the 5 rd day, and then gradually returned to normal levels in DRG; β-1,4-GalT-I and TNF-α were expressed in DRG neurons and glial cells, and the expression of β-1,4-GalT-I and TNF-α in the 5 rd day DRG neurons and glial cells in the experimental group was significantly higher than that in the control group; There was colocalization between β-1,4-GalT-I and TNF-α and MAPK signaling pathways were also activated in DRG of the experimental group.Conclusion: Inflammation of LFA in rats can lead to increased expression of β-1,4-GalT-I and TNF-α in DRG neurons and glial cells, which may be closely associated with the neurological symptoms of lower limbs caused by LFA.更多还原