摘要
目的:探讨卡托普利对高血压大鼠心脏钙调蛋白磷酸酶(calcineurin)、核因子κBp65(NFκBp65)蛋白表达影响及其机制。方法:建立腹主动脉缩窄高血压大鼠模型,术后1周用卡托普利治疗,连续10周。以尾动脉测压法观察血压变化,用免疫组织化学和形态计量学方法,观察calcineurin、NF-κBp65在心脏表达和心脏系数的变化。结果:经卡托普利治疗,高血压大鼠血压降低(mmHg,P<0.01),心脏系数显著减小(g/100g,P<0.01),心脏calcineurin和NF-κBp65蛋白高表达下调,阳性表达面积和面积百分比缩小(μm2,P<0.01,或P<0.01)。结论:卡托普利能通过调控信号转导通路calcineurin-NFAT-NF-κBp65关键蛋白表达,逆转高血压心血管重构。
AIM: To study the effect of captopril on ealcineurin and NF - κB p65 in the signal transduction pathway of the cardiovascular remodeling in hypertensive rats. METHODS: Using a animal model of hypertension induced by abdominal aortic banding, the mrs were treated with captopril for 10 weeks. The blood pressure was observed with a tail cuff method. The heart weight and heart weight/body weight were measured. The expression of caleineurin and NF - κB p65 were studied by using immunohistochemistry. RESULTS: After treated with captopril, the blood pressure of the model rats was decreased (P 〈0. 01 ), the heart weight or heart weight/body weight were also decreased (P 〈0. 01 ). The calci- neurin and NF - κB p65 protein overexpression was down - regulated, NF - κB - positive area and area percentage were reduced in the heart of hypertensive rats (P 〈0. 01 ,P 〈0. 01 ). CONCLUSION: Captopril reverses the cardiovascular remodeling by affecting the overexpression of calcineurin and NF - κB p65 involved in the cardiovascular remodeling in hypertensive rats.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2007年第1期40-43,共4页
Chinese Journal of Pathophysiology
基金
国家重点研究发展计划(973计划)基金资助项目(No.TG2000056901)