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目的:探索坐骨神经分支选择性损伤诱导的早期神经病理性疼痛(SNI)模型中给予糖皮质激素受体(glucocorticoid receptor,GR)激动剂对痛行为及促炎因子IL-6、TNF-α分泌的影响。方法:成年雄性SD大鼠随机均分为四组:Sham+Vehicle(生理盐水组),SNI+Vehicle组,SNI+DEX(GR激动剂地塞米松)组,SNI+RU(GR抑制剂米非司酮)组。Von Frey纤维丝检测各组大鼠缩足阈值(paw withdrawal threshold,PWT)的变化;Western Blot和免疫荧光染色检测各组脊髓中GR的表达水平;Elisa检测血清IL-6和TNF-α表达变化。结果:与SNI+Vehicle组比较,SNI+DEX组大鼠PWT阈值和脊髓GR的表达增高(P<0.05),血清IL-6和TNF-α浓度降低(P<0.05);SNI+RU组大鼠PWT阈值和脊髓GR表达降低(P<0.05),血清IL-6和TNF-α浓度升高(P<0.05)。结论:GR在脊髓水平能够通过下调促炎因子IL-6和TNF-α的表达缓解SNI诱导的早期神经病理性疼痛。
Objective: To explore the effect of glucocorticoid receptor (GR) agonist on the pain behavior and the secretion of pro-inflammatory cytokines IL-6 and TNF-α in early neuropathic pain (SNI) model induced by selective sciatic nerve branch injury . Methods: Adult male SD rats were randomly divided into four groups: Sham + Vehicle group, SNI + Vehicle group, SNI + DEX group (GR agonist dexamethasone group), SNI + RU Division ketone) group. Von Frey fiber was used to detect the change of paw withdrawal threshold (PWT) in each group. The expression of GR in each group was detected by Western Blot and immunofluorescence staining. The expression of IL-6 and TNF- . Results: Compared with SNI + Vehicle group, the PWT threshold and GR expression in SNI + DEX group were significantly increased (P <0.05) and the concentrations of IL-6 and TNF- The threshold of PWT and the expression of GR in spinal cord decreased (P <0.05), and the concentrations of IL-6 and TNF-α in serum increased (P <0.05). CONCLUSIONS: GR can relieve SNI-induced early neuropathic pain at the spinal level by down-regulating the expression of pro-inflammatory cytokines IL-6 and TNF-α.