中国医学创新
中國醫學創新
중국의학창신
MEDICAL INNOVATION OF CHINA
2012年
36期
14-17
,共4页
实验性自身免疫性脑脊髓炎%多发性硬化%TIM-3%TIM-1%阿托伐他汀
實驗性自身免疫性腦脊髓炎%多髮性硬化%TIM-3%TIM-1%阿託伐他汀
실험성자신면역성뇌척수염%다발성경화%TIM-3%TIM-1%아탁벌타정
Experimental autoimmune encephalomyelitis%Multiple sclerosis%TIM-3%TIM-1%Atorvastatin
目的:观察阿托伐他汀对实验性自身免疫性脑脊髓炎(experimental autoimmune encephalomyelitis,EAE)Wistar 大鼠的发病情况、组织病理变化及脑组织内 T 细胞免疫球蛋白和黏液域蛋白-3(TIM-3)、T 细胞免疫球蛋白和黏液域蛋白-1(TIM-1)表达水平的影响.方法:将30只雌性 Wistar 大鼠随机分为佐剂组、EAE 组、阿托伐他汀组,以豚鼠脊髓匀浆(GPSCH)诱发制备大鼠 EAE 模型,并于给予 GPSCH当日开始1次/d 灌服0.1% PBS 溶液1.5 ml/只(佐剂组和 EAE 组)和含阿托伐他汀的0.1% PBS 溶液,1次/d,剂量为8 mg/(kg·d),连续13 d,观察 EAE 症状并评分,用逆转录-聚合酶链反应(RT-PCR)法检测 Tim-1 mRNA、Tim-3 mRNA 在脑组织中的表达.结果:阿托伐他汀组发病率降低、临床症状减轻,体重下降减少(P<0.05);与佐剂组比较,EAE 组 TIM-3 mRNA 明显上升(P<0.05),阿托伐他汀组TIM-3 mRNA 较 EAE 组明显下降(P<0.05);与佐剂组比较,EAE 组 TIM-1 mRNA 下降(P<0.05),阿托伐他汀组 TIM-1 mRNA 较 EAE 组上升(P<0.05).结论:EAE 大鼠 TIM-3上升,TIM-1下降,提示其在 EAE 发病机制中发挥作用,通过下调 TIM-3、上调 TIM-1的表达,可能是阿托伐他汀对 EAE 保护作用机制之一.
目的:觀察阿託伐他汀對實驗性自身免疫性腦脊髓炎(experimental autoimmune encephalomyelitis,EAE)Wistar 大鼠的髮病情況、組織病理變化及腦組織內 T 細胞免疫毬蛋白和黏液域蛋白-3(TIM-3)、T 細胞免疫毬蛋白和黏液域蛋白-1(TIM-1)錶達水平的影響.方法:將30隻雌性 Wistar 大鼠隨機分為佐劑組、EAE 組、阿託伐他汀組,以豚鼠脊髓勻漿(GPSCH)誘髮製備大鼠 EAE 模型,併于給予 GPSCH噹日開始1次/d 灌服0.1% PBS 溶液1.5 ml/隻(佐劑組和 EAE 組)和含阿託伐他汀的0.1% PBS 溶液,1次/d,劑量為8 mg/(kg·d),連續13 d,觀察 EAE 癥狀併評分,用逆轉錄-聚閤酶鏈反應(RT-PCR)法檢測 Tim-1 mRNA、Tim-3 mRNA 在腦組織中的錶達.結果:阿託伐他汀組髮病率降低、臨床癥狀減輕,體重下降減少(P<0.05);與佐劑組比較,EAE 組 TIM-3 mRNA 明顯上升(P<0.05),阿託伐他汀組TIM-3 mRNA 較 EAE 組明顯下降(P<0.05);與佐劑組比較,EAE 組 TIM-1 mRNA 下降(P<0.05),阿託伐他汀組 TIM-1 mRNA 較 EAE 組上升(P<0.05).結論:EAE 大鼠 TIM-3上升,TIM-1下降,提示其在 EAE 髮病機製中髮揮作用,通過下調 TIM-3、上調 TIM-1的錶達,可能是阿託伐他汀對 EAE 保護作用機製之一.
목적:관찰아탁벌타정대실험성자신면역성뇌척수염(experimental autoimmune encephalomyelitis,EAE)Wistar 대서적발병정황、조직병리변화급뇌조직내 T 세포면역구단백화점액역단백-3(TIM-3)、T 세포면역구단백화점액역단백-1(TIM-1)표체수평적영향.방법:장30지자성 Wistar 대서수궤분위좌제조、EAE 조、아탁벌타정조,이돈서척수균장(GPSCH)유발제비대서 EAE 모형,병우급여 GPSCH당일개시1차/d 관복0.1% PBS 용액1.5 ml/지(좌제조화 EAE 조)화함아탁벌타정적0.1% PBS 용액,1차/d,제량위8 mg/(kg·d),련속13 d,관찰 EAE 증상병평분,용역전록-취합매련반응(RT-PCR)법검측 Tim-1 mRNA、Tim-3 mRNA 재뇌조직중적표체.결과:아탁벌타정조발병솔강저、림상증상감경,체중하강감소(P<0.05);여좌제조비교,EAE 조 TIM-3 mRNA 명현상승(P<0.05),아탁벌타정조TIM-3 mRNA 교 EAE 조명현하강(P<0.05);여좌제조비교,EAE 조 TIM-1 mRNA 하강(P<0.05),아탁벌타정조 TIM-1 mRNA 교 EAE 조상승(P<0.05).결론:EAE 대서 TIM-3상승,TIM-1하강,제시기재 EAE 발병궤제중발휘작용,통과하조 TIM-3、상조 TIM-1적표체,가능시아탁벌타정대 EAE 보호작용궤제지일.
Objective: To observe atorvastatin on experimental autoimmune encephalomyelitis(Experimental Autoimmune Encephalomyelitis, EAE),the incidence of Wistar rats,histopathological changes and brain tissue T cell immunoglobulin and mucus domain protein-3(the TIM-3)T-cell immune globulin and mucus-domain protein -1(TIM-1)expression levels. Method: 30 female Wistar rats were randomly divided into three groups:the adjuvant group,EAE group,and atorvastatin statin group. The preparation of guinea pig spinal cord homogenate(GPSCH)induced rat EAE model, and give GPSCH at the beginning of the day once daily gavage 0.1% PBS solution 1.5 ml(adjuvant group and EAE group)containing atorvastatin 0.1%PBS solution,once a day. Dose of 8 mg/(kgod),for 13 consecutive days to observe the EAE symptoms and rate,using reverse transcription-polymerase chain reaction(RT-PCR)assay the expression of Tim-1 mRNA in Tim-3 mRNA in the brain tissue. Result: Atorvastatin atorvastatin group decreased incidence,clinical symptoms,reduced weight loss(P<0.05). The comparison with adjuvant group,EAE group the TIM-3 mRNA increased(P<0.05), atorvastatin the statin group the TIM-3 mRNA compared EAE group decreased(P<0.05). The comparison with adjuvant group,EAE group the TIM-1 mRNA decreased(P<0.05),atorvastatin the statin group the TIM-1 mRNA increased compared with the EAE group,and a statistically significant (P<0.05). Conclusion: TIM-3 increased and TIM-1 decreased in EAE rats,which suggests that atorvastatin plays a role in EAE pathogenesis. This may be a protection mechanism of atorvastatin for EAE.
