摘要
目的:探讨磷脂酰肌醇3激酶/蛋白激酶B(PI3K/Akt)信号转导通路是否参与心力衰竭(心衰)恶病质的发生。方法:通过使用异丙肾上腺素制备大鼠心衰恶病质模型,根据体重和心脏彩超结果将大鼠分为心衰恶病质组、心衰非恶病质组及对照组。采用ELISA法检测3组大鼠血清胰岛素、胰岛素样生长因子-1(IGF-1)浓度;采用免疫组织化学法检测3组大鼠心肌组织中p85、p-Akt的表达情况;采用RT-PCR法检测3组大鼠心肌组织中caspase9mRNA、Bcl-xl mRNA的表达情况。结果:1胰岛素水平:心衰恶病质组显著高于非恶病质组(P<0.05)和对照组(P<0.05),但心衰非恶病质组低于对照组(P<0.05);2IGF-1水平:心衰恶病质组低于非恶病质组(P<0.05),与对照组之间无显著差异(P>0.05),但心衰非恶病质组高于对照组(P<0.05);3心肌组织p85、p-Akt的表达情况:心衰恶病质组低于非恶病质组(P<0.05)和对照组(P<0.05),但心衰非恶病质组高于对照组(P<0.05);4心肌组织caspase9mRNA的表达情况:心衰恶病质组高于非恶病质组(P<0.05)和对照组(P<0.05),但心衰非恶病质组低于对照组(P<0.05);5心肌组织Bcl-xl mRNA的表达情况:心衰恶病质组低于非恶病质组(P<0.05)和对照组(P<0.05),但心衰非恶病质组高于对照组(P<0.05)。结论:在ISO所致的大鼠心衰恶病质体内存在胰岛素及生长激素抵抗,PI3K/Akt信号转导通路受到抑制,PI3K/Akt信号转导通路参与心衰恶病质的发生。
Objective：To explore whether the phosphoinositide 3-kinase/protein kinase B（PI3K/AKT）signaling pathway was related to the occurrence of isoproterenol（ISO）-induced cardiac cachexia.Method：The rat model with cardiac cachexia was administered with ISO of 180mg/kg·d via inguinal subcutaneous injection.The rats were divided into cardiac cachexia group,no cachexia group and control group,according to the changes of body weight and the echocardiography results.The levels of insulin and Insulin-like growth factor-1（IGF-1）in the serum of all rats were detected by enzyme-linked immunosorbent assay（ELISA）;the expression of p85 and p-Akt in the myocardial tissue of all rats were detected by immunohistochemical;the expression of caspase9 mRNA and Bcl-xl mRNA in the myocardial tissue of all rats were detected by reverse transcription polymerase chain reaction（RT-PCR）.Result：The levels of insulin in cardiac cachexia group was significantly higher than that in both no cachexia group and control group（P0.05）,but was lower in no cachexia group than the control group（P0.05）;the levels of IGF-1in cardiac cachexia group was lower than in the no cachexia group（P0.05）,the heart failure non cachexia group was higher than the control group（P0.05）,while there were no satistically significantly differernces between cardiac cachexia group and control group（P0.05）;the expression of p85 and p-Akt in the cardiac cachexia group was lower than those in both no cachexia group（P0.05）and control group（P0.05）,but was higher in the no cachexia group than the control group（P0.05）;the expression of caspase9 mRNA in the myocardial tissue of rats：in cardiac cachexia group was higher than in the heart failure non cachexia group（P0.05）and control group（P0.05）,but the heart failure non cachexia group was lower than the control group（P0.05）;he expression of Bcl-xl mRNA in the myocardial tissue of rats：in cardiac cachexia group was lower than in the heart failure non cachexia group（P
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2016年第6期585-590,共6页
Journal of Clinical Cardiology
基金
内蒙古自治区高等学校"青年科技英才支持计划"(No:NJYT-14-B21)
