脂联素在高血压致炎症和心肌纤维化中的作用  

The Role of Adiponectin(APN) in Hypertension Ⅱ Infusion-induced Cardiac Inflammation and Fibrosis

作　　者：尚冬升 边云飞[1] 杨慧宇[1] 杨慧月 李小雷[1] 

机构地区：[1]山西医科大学附属第二医院心内科,山西省太原市030000

出　　处：《中国动脉硬化杂志》2015年第5期464-468,共5页Chinese Journal of Arteriosclerosis

基　　金：国家自然科学基金项目(81170198)

摘　　要：目的探讨脂联素在高血压致炎症和心肌纤维化中的作用。方法选取纯合脂联素敲除鼠12只(APN-/-)和野生型小鼠(WT)12只,采用微量泵持续灌注血管紧张素Ⅱ(AngⅡ)[1500 ng/(kg·min),7天]建立高血压模型,对照组给予乙酸溶液微量泵灌注,连续灌注7天,实验随机分成4组,每组6只:野生型小鼠对照组(WT),野生型小鼠+血管紧张素Ⅱ组(WT+AngⅡ),APN-/-对照组(APN-/-),APN-/-+血管紧张素Ⅱ组(APN-/-+AngⅡ),采用小鼠无创血压计测定小鼠尾动脉血压,运用ELISA法检测血清中s ICAM-1、s VCAM-1、v WF的含量,心肌组织Masson染色观察心脏纤维化,α-SMA免疫组化法观察肌成纤维细胞的形成,HE染色观察炎症细胞浸润,Western blot法测定TGF-β、TNF-α蛋白表达。结果与WT组相比,WT+AngⅡ组第二天血压开始升高,连续监测7天,血压均明显升高(P<0.05),造模成功。与WT+AngⅡ组相比,APN-/-+AngⅡ组血压显著升高(P<0.05),炎症细胞浸润明显增多(P<0.05),s ICAM-1、s VCAM-1、v WF含量明显增加,TGF-β、TNF-α表达显著上调,α-SMA+肌成纤维细胞数量增多(P<0.05)。结论在高血压致心脏纤维化过程中,脂联素可能有保护血管内皮损伤,抑制炎症反应,进而抑制心脏纤维化。Aim To research the role of adiponectin( APN) in hypertension-induced cardiac inflammation and fibrosis. Methods Select 12 homozygous adiponectin knockout mice( APN- /-) and 12 wild-type mice( WT) to establish the hypertension model by using the trace of continuous infusion pump angiotensinⅡ( AngⅡ)( 1500 ng·min,7 d),and the control group was given the trace of pump infusion acetic acid solution and for 7 days. The experiment is divided into four groups at random: the control group of wild-type mice( WT,6),+ angiotensinⅡ group of wild type mice( WT + AngⅡ,6),APN- /-in the control group( APN- /-,6),APN- /-+ angiotensin Ⅱ( APN- /-+ AngⅡ,6),using noninvasive blood to pressure mice tail artery blood pressure,detecting the content of s ICAM 1,s VCAM 1 and v WF in serum by using the method of ELISA. Myocardial tissue masson staining was used to observe cardiac fibrosis,α-SMA immunohistochemical method to observe the formation of muscle fibroblasts,HE staining to observe the inflammatory cells infiltration,western blot method to measure TGF-β,TNF-αprotein expression. Results Compared with WT group,the blood pressure of WT + AngⅡ group begins to rise at the next day,and the blood pressure increases obviously( P < 0. 05) for seven consecutive days,which explains that the building is successful. Compared with WT + AngⅡ group,the blood pressure of APN- /-+ AngⅡ group increases obviously( P < 0. 05),inflammatory cells infiltration increases obviously( P < 0. 05),the content of s ICAM 1,s VCAM 1,v WF increases obviously,the expression of TGF-β and TNF-α is upregulated obviously,α-SMA + muscle fibroblast populations increase( P < 0. 05).Conclusion In the process of high blood pressure caused by cardiac fibrosis,adiponectin maybe protect vasc ular endothelium injury,inhibiting inflammatory reaction,thereby inhibiting cardiac fibrosis.

关 键 词：APN 血管紧张素Ⅱ 高血压 炎症 纤维化 

分 类 号：R544.1[医药卫生—心血管疾病]