心电与循环
心電與循環
심전여순배
Journal of Electrocardiology(China)
2014年
3期
233-234,257
,共3页
高血压%血管紧张素II%过氧化氢酶
高血壓%血管緊張素II%過氧化氫酶
고혈압%혈관긴장소II%과양화경매
Hypertension%AngiotentionⅡ%Catalase
目的:探讨血管紧张素II(AngII)对大鼠血管过氧化氢酶(CAT)表达的影响。方法利用AngII微泵灌注制备高血压大鼠模型,分为AngII组、生理盐水组、对照组,每组6只。分别检测0、3、7、14d后各组大鼠尾动脉收缩压;连续灌注14d后,取材观察各组大鼠血管形态学改变;并采用免疫组化法检测各组大鼠颈动脉血管中CAT及氧化应激产物4-羟烯酸(4HNE)蛋白的表达情况。结果与生理盐水组及对照组相比,AngII灌注后能够显著提高大鼠尾动脉收缩压水平及颈动脉血管中膜厚度(均P<0.01);免疫组化显示AngII组颈动脉血管CAT表达显著降低,而4HNE表达显著增加(均P<0.01)。结论 Ang II可下调大鼠血管中CAT表达而导致氧化应激的发生。
目的:探討血管緊張素II(AngII)對大鼠血管過氧化氫酶(CAT)錶達的影響。方法利用AngII微泵灌註製備高血壓大鼠模型,分為AngII組、生理鹽水組、對照組,每組6隻。分彆檢測0、3、7、14d後各組大鼠尾動脈收縮壓;連續灌註14d後,取材觀察各組大鼠血管形態學改變;併採用免疫組化法檢測各組大鼠頸動脈血管中CAT及氧化應激產物4-羥烯痠(4HNE)蛋白的錶達情況。結果與生理鹽水組及對照組相比,AngII灌註後能夠顯著提高大鼠尾動脈收縮壓水平及頸動脈血管中膜厚度(均P<0.01);免疫組化顯示AngII組頸動脈血管CAT錶達顯著降低,而4HNE錶達顯著增加(均P<0.01)。結論 Ang II可下調大鼠血管中CAT錶達而導緻氧化應激的髮生。
목적:탐토혈관긴장소II(AngII)대대서혈관과양화경매(CAT)표체적영향。방법이용AngII미빙관주제비고혈압대서모형,분위AngII조、생리염수조、대조조,매조6지。분별검측0、3、7、14d후각조대서미동맥수축압;련속관주14d후,취재관찰각조대서혈관형태학개변;병채용면역조화법검측각조대서경동맥혈관중CAT급양화응격산물4-간희산(4HNE)단백적표체정황。결과여생리염수조급대조조상비,AngII관주후능구현저제고대서미동맥수축압수평급경동맥혈관중막후도(균P<0.01);면역조화현시AngII조경동맥혈관CAT표체현저강저,이4HNE표체현저증가(균P<0.01)。결론 Ang II가하조대서혈관중CAT표체이도치양화응격적발생。
Objective To investigate the effects of Angiotensin (Ang)Ⅱon the expression of catalase of rat vessels. Methods 18 rats were randomly divided into Ang II group (n=6)infused with Ang II by micro- pump and saline group (n=6) infused with saline for 14 days, and control group(n=6). Systolic pressure of tail artery was measured at 0,3,7 and 14 day. The rats were sacrificed for observing vessel morphological changes at 14th day. Catalase and oxidative stress product- 4HNE were determined by immunohistochemistry. Results Systolic blood pressure of tail artery as wel as the thickness of carotid artery media increased significantly, Catalase was significantly lower while oxidative stress product- 4HNE was higher in Ang II group compared to control group (al P<0.01). Conclusion AngⅡ may promote oxidative stress through inhibiting catalase expression of rat vessels.