陕西医学杂志
陝西醫學雜誌
협서의학잡지
SHAANXI MEDICAL JOURNAL
2014年
12期
1571-1573,1578
,共4页
袁海峰%牛小麟%高登峰%郝光华%宋安琪%魏瑾
袁海峰%牛小麟%高登峰%郝光華%宋安琪%魏瑾
원해봉%우소린%고등봉%학광화%송안기%위근
动脉%过氧化物酶体类%罗格列酮%动物,实验%大鼠
動脈%過氧化物酶體類%囉格列酮%動物,實驗%大鼠
동맥%과양화물매체류%라격렬동%동물,실험%대서
Artery%Perozidases%Rosiglitazone Animals,laboratory%Rats
目的:探讨老龄SHR大鼠胸主动脉过氧化物酶体增殖物激活受体γ( PPARγ)表达变化情况及罗格列酮(Ros)干预作用。方法:64周龄Wistar‐Kyoto(WKY)大鼠和自发性高血压大鼠( SHR)分为WKY ,SHR及SHR+Ros组,每组9只。SHR+Ros组大鼠给予Ros(5mg/kg/d)灌胃,连续56d;WKY和SHR组大鼠分别灌服等体积的生理盐水。干预结束后采用tail cuff法测量各组大鼠尾动脉收缩压,采用HE染色观察主动脉组织病理学改变情况,采用免疫组化染色及图像分析检测胸主动脉PPARγ蛋白表达情况,采用real time‐PCR检测主动脉PPARγ mRNA表达情况。结果:与WKY大鼠相比,SHR大鼠血压升高(P<0.05),HE染色可见胸主动脉管壁增厚,内弹力板变直,间质增厚,细胞核着色较淡,免疫组化染色及real time‐PCR结果表明SHR大鼠胸主动脉PPARγ蛋白及mRNA表达水平均下降(均 P<0.05),与SHR组相比,SHR+Ros组大鼠血压降低(P<0.05),胸主动脉组织病理学改变情况缓解,管壁变薄,内弹力板趋于迂曲,间质变薄,细胞核着色变深,PPARγ蛋白及mRNA表达水平均增加(P<0.05)。结论:老龄SHR大鼠胸主动脉存在PPARγ表达下降,PPARγ配体罗格列酮可以逆转这种现象。
目的:探討老齡SHR大鼠胸主動脈過氧化物酶體增殖物激活受體γ( PPARγ)錶達變化情況及囉格列酮(Ros)榦預作用。方法:64週齡Wistar‐Kyoto(WKY)大鼠和自髮性高血壓大鼠( SHR)分為WKY ,SHR及SHR+Ros組,每組9隻。SHR+Ros組大鼠給予Ros(5mg/kg/d)灌胃,連續56d;WKY和SHR組大鼠分彆灌服等體積的生理鹽水。榦預結束後採用tail cuff法測量各組大鼠尾動脈收縮壓,採用HE染色觀察主動脈組織病理學改變情況,採用免疫組化染色及圖像分析檢測胸主動脈PPARγ蛋白錶達情況,採用real time‐PCR檢測主動脈PPARγ mRNA錶達情況。結果:與WKY大鼠相比,SHR大鼠血壓升高(P<0.05),HE染色可見胸主動脈管壁增厚,內彈力闆變直,間質增厚,細胞覈著色較淡,免疫組化染色及real time‐PCR結果錶明SHR大鼠胸主動脈PPARγ蛋白及mRNA錶達水平均下降(均 P<0.05),與SHR組相比,SHR+Ros組大鼠血壓降低(P<0.05),胸主動脈組織病理學改變情況緩解,管壁變薄,內彈力闆趨于迂麯,間質變薄,細胞覈著色變深,PPARγ蛋白及mRNA錶達水平均增加(P<0.05)。結論:老齡SHR大鼠胸主動脈存在PPARγ錶達下降,PPARγ配體囉格列酮可以逆轉這種現象。
목적:탐토노령SHR대서흉주동맥과양화물매체증식물격활수체γ( PPARγ)표체변화정황급라격렬동(Ros)간예작용。방법:64주령Wistar‐Kyoto(WKY)대서화자발성고혈압대서( SHR)분위WKY ,SHR급SHR+Ros조,매조9지。SHR+Ros조대서급여Ros(5mg/kg/d)관위,련속56d;WKY화SHR조대서분별관복등체적적생리염수。간예결속후채용tail cuff법측량각조대서미동맥수축압,채용HE염색관찰주동맥조직병이학개변정황,채용면역조화염색급도상분석검측흉주동맥PPARγ단백표체정황,채용real time‐PCR검측주동맥PPARγ mRNA표체정황。결과:여WKY대서상비,SHR대서혈압승고(P<0.05),HE염색가견흉주동맥관벽증후,내탄력판변직,간질증후,세포핵착색교담,면역조화염색급real time‐PCR결과표명SHR대서흉주동맥PPARγ단백급mRNA표체수평균하강(균 P<0.05),여SHR조상비,SHR+Ros조대서혈압강저(P<0.05),흉주동맥조직병이학개변정황완해,관벽변박,내탄력판추우우곡,간질변박,세포핵착색변심,PPARγ단백급mRNA표체수평균증가(P<0.05)。결론:노령SHR대서흉주동맥존재PPARγ표체하강,PPARγ배체라격렬동가이역전저충현상。
Objectives:To investigate the expression of peroxisome proliferators‐activated receptor γ(PPARγ) in the thoracic aorta of spontaneously hypertensive rats (SHR) with age and the inhibitory effect of rosigl‐itazone (Ros) on the expression of PPARγ.Methods :64‐week old wistar‐Kyoto rats (WKY) and SHR were ran‐domly and respectively divided into WKY ,SHR and SHR+ Ros group ,with 9 rats in each group .The rats in SHR+ Ros group were treated with Ros (5 mg/kg ,intragastrically) for 56 days ,whereas normal saline was applied in WKY and SHR groups .Systolic blood pressure (SBP) of rats was measured by tail cuff method .Histopathological damage of thoracic aorta was analyzed by Hematoxylin‐eosin (HE) staining .The levels of PPARγprotein and mR‐NA of thoracic aorta were detected by immunohistochemistry staining and real time‐PCR respectively .Results :Com‐pared with the rats in WKY group ,the SBP of rats in SHR group was higher (P<0 .05) ,and the levels of PPARγprotein and mRNA in thoracic aorta of rats in SHR group were lower respectively (P<0 .05) .In addition ,HE stai‐ning revealed some remarkable histopathological abnormalities in thoracic aorta of rats in SHR group .The thickness of thoracic aorta was increased ,and the elastic fiber was straight ,and the interstitium between elastic fibers become thick ,and the nucleuses were stained by hematoxylin slightly .Compared with the rats in SHR group ,the SBP of rats in SHR+Ros group was lower (P<0 .05) ,and the histopathological abnormalities in thoracic aorta were atten‐uated .The thickness of thoracic aorta was decreased ,and the elastic fiber was twisted ,and the interstitium between elastic fibers become thin ,and nucleus could be stained by hematoxylin deeply .Furthermore ,the levels of PPARγprotein and mRNA in thoracic aorta of rats in SHR group were higher than those in SHR group respectively (P<0 . 05) .Conclusion:The expression of PPARγin the thoracic aorta of SHR with age is decreased while thoracic aorta is aging ,and rosiglitazone can play an inhibitory effect .