摘要
目的研究糖蛋白130(GP130)在腹主动脉缩窄所致大鼠压力超负荷性心肌肥大模型中的表达变化与心肌肥大的关系,以及贝那普利(Benazepril,Ben)对GP130蛋白表达及心肌肥大的影响。方法用腹主动脉缩窄术建立大鼠压力超负荷性心肌肥厚模型,随机分为左室肥厚组(LVH,n=7)、贝那普利干预组(n=7,贝那普利1mg.kg-1.d-1,灌胃3周),另设一假手术组(n=7)为对照。干预3周后测定血流动力学指标、左心室质量指数,应用放射免疫分析法测定心肌血管紧张素Ⅱ(AngⅡ)水平,免疫组化法检测心肌中GP130蛋白水平表达。结果与假手术组比较,左室肥厚组动物的血压与左心室质量指数显著升高(P<0.05);心肌组织AngⅡ含量(P<0.01)和GP130蛋白表达水平明显增加(P<0.05)。贝那普利干预可显著降低血压和左心室质量指数(P<0.05),同时降低肥厚心肌组织AngⅡ浓度(P<0.01)与GP130蛋白表达水平(P<0.05)。结论GP130蛋白的过度表达参与了压力超负荷性大鼠心肌肥大的发病过程;贝那普利对GP130蛋白表达及心肌肥大有抑制作用。
Objective To investigate the changes of GP130 expression in rats with pressure overload-induced cardiac hypertrophy, and the effect of Benazepril on GP130 expression and the concerned cardiac hypertrophy. Methods Two weeks after the Wistar rat model of pressure overload was established by constriction of abdominal aorta, the survived rats were randomly divided into hypertrophy group （ LVH, n = 7） and Benazepril intervention group （ Ben, n = 7, 1 mg · kg^-1 · d^-1 Benazepril orally for 3 weeks）. A sham-operation group （Sham, n = 7） was set up as control. Blood pressure and left ventricular mass index （LVMI） were investigated at 3th week after model establishment. Ang Ⅱ level in myocardium was measured by radioimmunoassay. The protein level of GP130 in cardiomyocytes was determined by immunohistochemistry. Results As compared with the Sham group, blood pressure and LVMI increased significantly （ P 〈 0.05 ） ; the level of Ang Ⅱ （ P 〈 0. 01 ） and the GP130 expression （P 〈0.05） were enhanced significantly. Benazepril decreased blood pressure, LVMI, Ang Ⅱ level （P 〈 0.01 ） and the GP130 expression （P 〈 0.05 ） significantly as compared to those of LVH group. Conclusion The overexpression of GP130 may play an important role in cardiac hypertrophy. Benazepril may decrease the GP130 expression and inhibit cardiac hypertrophy.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2006年第20期2027-2029,共3页
Journal of Third Military Medical University
基金
国家自然科学基金资助项目(30000071)~~
