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The Protection of Peroxisome Proliferators Activated Receptor-gamma Agonist Against Focal Cerebral Ischemia-reperfusion Injury in Mice

Author: ShangJinLin
Tutor: ChengZuo;SunLi
School: Tianjin Medical University
Course: Neurology
Keywords: Peroxisome proliferator-activated receptor γ agonist Brain Ischemia-reperfusion injury Inflammation Mice
CLC: R743.3
Type: PhD thesis
Year: 2009
Downloads: 257
Quote: 0
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Abstract


Purpose of peroxisome proliferator-activated receptor γ (peroxisome proliferator-activatedreceptor gamma, PPARγ) is a way to regulate a variety of inflammatory mediators expressed nuclear transcription factor activated organs outside the brain ischemia reperfusion injury The protective effect. Our experimental observation of PPARγ agonists on mice with focal cerebral ischemia-reperfusion injury protection, and a preliminary study of its mechanism. The method of production in the mouse brain artery occlusion and reperfusion model (MCAO / R), given 1 h before ischemia PPARγ agonist rosiglitazone (Rosiglitazone) intervention the 0mg/kg (control group, were randomly divided into different basis for intervention dose ), 3mg/kg the, 6mg/kg group, and 12mg/kg group (n = 10). 3% triphenyltetrazolium chloride (2,3,5-triphenyltetrazolium TTC) staining, nerve function defect scores were used to observe the PPARγ agonist rosiglitazone mouse infarct volume and behavioral Preliminary screening optimal interventions dose. MCAO / R model and then apply the dose of the intervention of the different time points, according to different intervention point in time, that is before ischemia, 1 h, at the same time, after ischemia, 1 h, 2 h after ischemia and after ischemia for 3 h of ischemia randomization. Were assayed infarct volume TIC staining; Zea-Longa rated method of the mice in each group ethology assessment; ultraviolet spectrophotometry detection of brain tissue myeloperoxidase enzyme (myeloperoxidase, MPO) activity; RT- PCR detection of inflammatory factors (ICAM-1, IL-1β, COX-2) mRNA expression levels; immunohistochemistry, Western-blot was used to observe the protein expression of the inflammatory cytokines. Results (1) Compared with cerebral infarction control group, PPARγ agonist rosiglitazone 3mg/kg intervention group, infarct volume in mice 6mg/kg intervention group and the the 12mg/kg intervention group was significantly reduced (F = 65.551 , P <0.01); behavior scores, compared to the control group and cerebral infarction, PPARγ agonist rosiglitazone 3mg/kg intervention group, 6mg/kg intervention group and the 12mg/kg intervention group mice motor score reducing (F = 6.451, P <0.01). To which rosiglitazone 6mg/kg intervention group, 12mg/kg intervention group infarct volume and behavioral score was better than 3mg/kg intervention group were statistically significant (P <0.05), while the 6mg/kg intervention group and 12mg/kg intervention group between the two groups did not show significant difference (P> 0.05); (2) select 6mg/kg dose administered intervention grouped in a different point in time (where A was the control group, B group 1 h after ischemia administration group administered 1 h before ischemia group, C group ischemia administration group, D group, E group 2 h after ischemia the administered group F group for ischemic 3 h dose group), the results show: 1 infarct volume: Compared with group A, group B and group C were able to significantly reduce the mouse infarct volume (F = 23.407, P <0.01), D , E, F group were not statistically different; ② behavioral rating: Compared with group A, group B and group C were able to significantly reduce the mouse behavior scores (F = 8.355, P <0.01) , D, E, F group were not statistically different; ③ MPO value: Compared with group A, group B and C group mice ischemic brain tissue MPO activity was significantly lower (F = 20.907, P <0.01 above inflammatory), D, E, F group had no significant difference; ④ inflammatory cytokines of ICAM-1, IL-1β and COX-2 mRNA expression: Compared with group A, group B and group C ischemic brain tissue factor gene expression levels were significantly lower (F values ??were 15.907,12.354,16.282, P <0.01), D, E, F group were not statistically different; ⑤ inflammatory cytokines ICAM- 1, IL-1β and COX-2 protein expression level: Compared with group A, group B and group C ischemic brain tissue of the inflammatory factor protein expression levels were significantly lower (F values ??were 33.561,22.304 , 19.207, P <0.01), D, E, F group were not statistically different. Conclusion (1) PPARγ agonists have a protective effect on brain ischemia and reperfusion injury. (2) PPARγ agonists on brain ischemia and reperfusion injury protection mechanism with the suppression of the inflammatory response of the ischemic brain tissue. (3) PPARγ agonists in brain ischemia-reperfusion injury early application.

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CLC: > Medicine, health > Neurology and psychiatry > Neurology > Cerebrovascular disease > Acute cerebrovascular disease ( stroke)
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