复心合剂对心衰大鼠信号通路Raf-MEK-ERK的影响  

The Effect of Fuxin Mixture on Raf-MEK-ERK Pathway in Chronic Congestive Heart Failure( CHF) Rats

作　　者：薛一涛[1] 李秋实 焦华琛[1] 苏文革[1] 

机构地区：[1]山东中医药大学附属医院,山东济南250000 [2]北京王府中西医结合医院,北京102200

出　　处：《中华中医药学刊》2015年第4期791-794,共4页Chinese Archives of Traditional Chinese Medicine

基　　金：国家自然科学基金项目(81273703)

摘　　要：目的:初步探索复心合剂对信号通路Raf-MEK-ERK的影响。方法:75只Wistar雄性大鼠,随机分为5组,对照组、卡托普利组、复心合剂低剂量组、复心合剂高剂量组均为15只。实验过程中阿霉素干预4周后测定大鼠心功能;6周后应用Western blot法检测大鼠心肌组织中Raf、MEK、ERK蛋白表达情况。结果:(1)与正常对照组比较,模型组大鼠BNP值显著升高(P<0.01),心衰模型成功建立。(2)与正常对照组相比,模型组大鼠心肌组织Raf水平显著升高(P<0.01),复心合剂高剂量组、卡托普利组大鼠心肌组织Raf水平显著降低(P<0.01),与卡托普利组相比,复心汤高剂量组大鼠心肌组织Raf无统计学意义(P>0.05)。(3)与正常对照组相比,模型组大鼠心肌组织MEK水平显著升高(P<0.01),复心合剂高剂量组、卡托普利组大鼠心肌组织MEK水平显著降低(P<0.01)。(4)与正常对照组相比,模型组大鼠心肌ERK蛋白表达明显升高(P<0.01),卡托普利组及复心合剂高剂量组ERK蛋白表达无显著差异性(P>0.05),与模型组相比,复心合剂高剂量组、卡托普利组大鼠心肌组织ERK水平显著降低(P<0.01)。结论:复心合剂对心衰大鼠信号通路Raf-MEK-ERK的蛋白激活具有一定的抑制作用,延缓心衰进程。Objective： To study the effect of Fuxin mixture on Raf-MEK-ERK pathway in Chronic congestive Heart Failure（ CHF） rats. Methods： 75 male wistar rats are randomly divided into 5 groups： control group,model group,captopril group,Fuxin mixture low dose group and Fuxin mixture high dose group. Adriamycin cardiotoxicity was utilized to induce rat heart failure model. Cardiac function was detemined after 4 weeks,and Western blotting was used to detect protein expression of Raf、MEK、ERK in myocardial tissue of rats. Results：（ 1） BNP of model group increased significantly compared with control group（ P〈0. 01）,which indicated the model was successfully build up.（ 2） Compared with control group,Raf in myocardial tissue of model group increased significantly（ P〈0. 01）,while decreased significantly（ P〈0. 01） of captopril group and Fuxin mixture high dose group. The difference of Raf between captopril group and Fuxin mixture high dose group was not stastically significant.（ 3） Compared with control group,MEK in myocardial tissue of model group increased significantly（ P〈0. 01）,while decreased significantly（ P〈0. 01） of captopril group and Fuxin mixture high dose group.（ 4） Compared with control group,ERK in myocardial tissue of model group increased significantly（ P〈0. 01）,while the difference of ERK between captopril group and Fuxin mixture high dose group was not stastically significant（ P〉0. 05）. Compared with model group,ERK of captopril group and Fuxin mixture high dose group decreased significantly（ P〈0. 01）. Conclution： The Fuxin mixture can someway inhibited Raf / MEK / ERK signaling to delay the process of heart failure.

关 键 词：复心合剂 心力衰竭 信号通路 Raf/MEK/ERK 

分 类 号：R285.5[医药卫生—中药学]