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1. 重庆医科大学附属第一医院神经内科重庆市神经病学重点实验室
2. 重庆医科大学附属第一医院神经内科重庆市神经病学重点实验室,重庆,400016
纸质出版日期:2007,
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[1]袁宝玉,秦新月,彭国光.PPAR-γ激动剂对急性EAE大鼠脑白质TNF-αmRNA表达的影响[J].重庆医科大学学报,2007(01):18-21.
YUAN Baoyu, et al. Effects of peroxisome proliferator-actived receptors-γ agonists on tumor necrosis factor-α expression in rats with acute experimental autoimmune encephalomyelitis[J]. Journal of Chongqing Medical University, 2007,(1):18-21.
[1]袁宝玉,秦新月,彭国光.PPAR-γ激动剂对急性EAE大鼠脑白质TNF-αmRNA表达的影响[J].重庆医科大学学报,2007(01):18-21. DOI:
YUAN Baoyu, et al. Effects of peroxisome proliferator-actived receptors-γ agonists on tumor necrosis factor-α expression in rats with acute experimental autoimmune encephalomyelitis[J]. Journal of Chongqing Medical University, 2007,(1):18-21. DOI:
目的:探讨过氧化物酶体增殖物激活受体-γ(peroxisomeproliferator-activedreceptors-γ
PPAR-γ)激动剂罗格列酮和非甾体类抗炎药布洛芬对实验性自身免疫性脑脊髓炎(experimentalautoimmuneencephalomyelitis
EAE)大鼠肿瘤坏死因子-α(tumornecrosisfactor-α
TNF-α)表达的影响。方法:建立大鼠EAE模型
分别给予罗格列酮和布洛芬预处理
通过各组间临床表现评分评价药物疗效
RT-PCR法检测TNF-αmRNA的表达。结果:与EAE模型组大鼠相比
罗格列酮和布洛芬治疗组的症状明显改善
罗格列酮和布洛芬治疗组TNF-αmRNA表达较EAE模型组明显下调(P<0.01)。两个治疗组间的各项指标间比较无明显差异(P>0.05)。结论:罗格列酮和布洛芬明显改善EAE大鼠的临床表现
下调前炎症细胞因子TNF-αmRNA的表达。提示PPAR-γ激动剂对EAE或多发性硬化(multiplesclerosis
MS)具有抗炎的神经保护作用
布洛芬在EAE中的抗炎作用可能与激活PPAR-γ有关。
Objective:To explore the effects of peroxisome proliferator-actived receptors-γ(PPAR-γ)agonists rosiglitazone and non-steroidal anti-inflammatory drugs(NSAIDs) ibuprofen on tumor necrosis factor-α(TNF-α)mRNA expression in the brain of rats with acute experimental autoimmune encephalomyelitis(EAE).Methods:EAE models on rat were established by inoculating the homogenate containing spinal cord of guinea pig and complete Freund’s adjuvant
and then treated by rosiglitazone and ibuprofen respectively.The improvement of clinical manifestations was assessed to determine the curative effect of the two medicines and TNF-α mRNA expression level was detected by RT-PCR.Results:Compared with EAE group
the groups with rosiglitazone and ibuprofen showed improvement in clinical manifestations
and the expression of TNF-α mRNA reduced markedly(P<0.01).Other index of the treated groups were no significantly different(P>0.05).Conclusions:PPAR-γ agonists rosiglitazone and NSAIDs ibuprofen could obviusely improve the clinical manifestations of EAE rats
and decrease the level of the expression of TNF-α mRNA
which suggested PPAR-γ agonists may have the anti-inflammation neural protective function on EAE or multiple sclerosis(MS)
and the anti-inflammation of ibuprofen may be related to the activation of PPAR-γ.
实验性自身免疫性脑脊髓炎肿瘤坏死因子过氧化物酶体增殖物激活受体-γ非甾体类抗炎药
Experimental autoimmune encephalomyelitis(EAE)Tumor necrosis factor-α(TNF-α)Peroxisome proliferator-activated receptor-γ(PPAR-γ)NSAIDs.
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