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目的:探讨奈普生对大鼠实验性变应性脑脊髓炎(Experimental Allergic Encephalomyelitis,EAE)的治疗作用,观察其对大鼠脑组织中炎性标志物肿瘤坏死因子(Tumor necrosis factor-α,TNF-α) m RNA表达的影响。方法:采用免疫诱导方法制备EAE大鼠模型,分别予不同剂量的奈普生对其进行实验性干预治疗,对其神经功能缺损加以评分并计算其发病率,RT- PCR法半定量TNF- αm RNA的表达。结果:与EAE模型组相比,奈普生干预组大鼠的临床症状显著改善(P<0 .0 5 ) ,而其发病率与EAE模型组无显著性差异;RT- PCR结果显示,奈普生干预组TNF- αm RNA的表达较EAE模型组明显降低(P<0 .0 5 ) ;神经功能缺损评分的改善和TNF- αm RNA的表达的降低均以低剂量奈普生治疗组为显著(P<0 .0 1)。结论:奈普生能够显著改善EAE的临床症状,并且能够抑制EAE脑白质的TNF-αm RNA的表达,特别是小剂量的奈普生对EAE具有更为明显的抗炎作用,可能奈普生具有过氧化物酶体增殖激活受体-γ(Peroxi-some proliferator- activated receptor- γ,PPAR- γ)激动作用。
Objective: To investigate the therapeutic effect of Naproxen on experimental Allergic Encephalomyelitis (EAE) in rats and to observe its effect on the expression of Tumor necrosis factor-α TNF-α) m RNA expression. Methods: The rat model of EAE was induced by immune induction. Naproxen was administered to different doses of Naproxen for experimental intervention. The neurological deficits were scored and their incidences were calculated. Semi-quantitative RT-PCR for TNF-αm RNA expression. Results: Compared with the EAE model group, the clinical symptoms of the rats treated with Naproxen were significantly improved (P <0.05), while the incidence of EAE was no significant difference. The results of RT-PCR Compared with EAE model group, the expression of TNF-αmRNA in normal students was significantly lower than that in EAE model group (P <0.05); the improvement of neurological deficit score and the decrease of TNF-αmRNA expression were observed in low-dose naproxen-treated group Significant (P <0.01). CONCLUSION: Naproxen can significantly improve the clinical symptoms of EAE and inhibit the expression of TNF-αmRNA in EAE white matter. In particular, Naproxen has a more pronounced anti-inflammatory effect on EAE, It has the activation of peroxisome proliferator-activated receptor-γ (PPAR-γ).