脑与神经疾病杂志
腦與神經疾病雜誌
뇌여신경질병잡지
JOURNAL OF BRAIN AND NERVOUS DISEASES
2014年
2期
86-89
,共4页
祝春华%杨燚%温雅%崔海瑛%张祥建
祝春華%楊燚%溫雅%崔海瑛%張祥建
축춘화%양일%온아%최해영%장상건
脑缺血%基质金属蛋白酶-9%过氧化物酶体增殖物激活受体γ%替米沙坦
腦缺血%基質金屬蛋白酶-9%過氧化物酶體增殖物激活受體γ%替米沙坦
뇌결혈%기질금속단백매-9%과양화물매체증식물격활수체γ%체미사탄
Cerebral ischemia%Matrix metalloproteinases-9%Peroxisome proliferator-activated receptor gamma%Telmisartan
目的:探讨MMP-9在大鼠脑缺血性损伤中的作用以及替米沙坦对MMP-9表达的调控机制。方法线栓法建立大鼠右侧大脑中动脉闭塞( MCAO)模型。实验大鼠分为假手术组、溶剂对照组、替米沙坦组、替米沙坦+GW9662组。采用免疫组化、Western blot和qR-T PCR来观察脑缺血后24 h MMP-9和PPARγ的mRNA和蛋白表达变化,TTC染色评价脑梗死体积,干湿重法评价患侧脑水肿。结果替米沙坦能够明显上调PPARγ,下调 MMP-9表达,改善神经功能缺失,减轻脑水肿,减小梗死体积。 PPARγ特异性阻断剂GW9662能够阻断该作用,保护作用消失。结论 MMP-9在缺血性脑损伤中发挥重要作用,替米沙坦通过激活PPARγ抑制MMP-9表达对脑缺血性脑组织发挥保护作用。
目的:探討MMP-9在大鼠腦缺血性損傷中的作用以及替米沙坦對MMP-9錶達的調控機製。方法線栓法建立大鼠右側大腦中動脈閉塞( MCAO)模型。實驗大鼠分為假手術組、溶劑對照組、替米沙坦組、替米沙坦+GW9662組。採用免疫組化、Western blot和qR-T PCR來觀察腦缺血後24 h MMP-9和PPARγ的mRNA和蛋白錶達變化,TTC染色評價腦梗死體積,榦濕重法評價患側腦水腫。結果替米沙坦能夠明顯上調PPARγ,下調 MMP-9錶達,改善神經功能缺失,減輕腦水腫,減小梗死體積。 PPARγ特異性阻斷劑GW9662能夠阻斷該作用,保護作用消失。結論 MMP-9在缺血性腦損傷中髮揮重要作用,替米沙坦通過激活PPARγ抑製MMP-9錶達對腦缺血性腦組織髮揮保護作用。
목적:탐토MMP-9재대서뇌결혈성손상중적작용이급체미사탄대MMP-9표체적조공궤제。방법선전법건립대서우측대뇌중동맥폐새( MCAO)모형。실험대서분위가수술조、용제대조조、체미사탄조、체미사탄+GW9662조。채용면역조화、Western blot화qR-T PCR래관찰뇌결혈후24 h MMP-9화PPARγ적mRNA화단백표체변화,TTC염색평개뇌경사체적,간습중법평개환측뇌수종。결과체미사탄능구명현상조PPARγ,하조 MMP-9표체,개선신경공능결실,감경뇌수종,감소경사체적。 PPARγ특이성조단제GW9662능구조단해작용,보호작용소실。결론 MMP-9재결혈성뇌손상중발휘중요작용,체미사탄통과격활PPARγ억제MMP-9표체대뇌결혈성뇌조직발휘보호작용。
Objective This study is to explore the role of MMP-9 in the focal cerebral ischemia of rats and the mechanisms of telmisartan regulating MMP-9 expression.Methods Male Sprague-Dawley rats were subjected to permanent middle cerebral artery occlusion (MCAO).SD rats were randomly divided into 4 groups:sham-operated group, vehicle group, telmisartan group, and telmisartan +GW9662 group.At 24h after focal cerebral ischemia,MMP-9 and PPARγexpression were explored by immunohistochemistry, Western blot and qR-T PCR.The brain edema was measured by dry-wet weight method, the infarct volume was detected by TTC stain.Results Telmisartan dramatically increased PPARγand decreased MMP-9 and alleviated the neurological deficits,brain water content and infarct volume after focal cerebral ischemia, which were all reversed by GW9662 administration.Conclusion MMP9-plays an important role in the second brain damage after focal cerebral ischemia.Telmisartan protects brain againsts ischemia by decreasing MMP-9 via activating PPARγ.