摘要
目的:探讨过氧化物体增殖剂激活的受体γ激动剂对大鼠实验性自身免疫性脑脊髓炎(EAE)的治疗作用,以及对其脑组织中钙激活的中性蛋白酶(calpain)表达的影响。方法:建立大鼠EAE动物模型,分别给予PPARγ激动剂罗格列酮和非甾体类抗炎药布洛芬预处理,通过各组间临床表现评分评价药物疗效,RT-PCR法检测calpain mRNA的表达,Western blotting法检测calpain蛋白表达水平。结果:罗格列酮和布洛芬治疗组大鼠的临床表现评分显著低于EAE模型组;3组间calpain mRNA表达水平无显著差异(P>0.05),但罗格列酮和布洛芬组calpain蛋白质的表达明显低于EAE模型组(P<0.05)。结论:PPARγ激动剂能够显著减轻EAE大鼠的临床症状,抑制calpain蛋白质的表达,表明PPARγ激动剂对实验性自身免疫性脑脊髓炎大鼠具有脑保护作用。
AIM: To explore the effects of peroxisome proliferator- activated receptor γ (PPARγ) agonist on calcium - activated neutral proteinase, calpain, expression in the brain of rats with acute experimental autoimmune encephalomyelitis (EAE). METHODS : EAE model was established in rats by inoculating the homogenate contained spinal cord of guinea pig and complete Freund's adjuvant. Respectively, the PPARγ agonist rosiglitazone and non - steroid anti - inflammatory drug (NSAID) ibuprofen were used to treat the EAE rats. Outcome measures (Koh's scale) were applied at baseline and after treatment to assess the improvement of clinical symptoms. Calpain expression levels were detected by RT - PCR and Western blotting. RESULTS : All the groups showed significant improvements of scales scores after treatment with rosiglitazone and ibuprofen. No significant difference of the expression of calpain mRNA was found among EAE group, rosiglitazone and ibuprofen groups ( P 〉 0.05 ), but the expression of calpain reduced markedly in rosiglitazone and ibuprofen groups compared with that in EAE group ( P 〈 0. 05 ). CONCLUSION : Rosiglitazone and ibuprofen inhibit the expression of calpain and improve the clinical symptoms of EAE rats. PPARγ agonist plays a neuroprotective role in EAE rats.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2007年第5期955-958,共4页
Chinese Journal of Pathophysiology
基金
重庆市自然科学基金资助项目[No.渝科委计(2001)54号文52]