超声微泡介导H-FABP基因改善慢性心衰大鼠的心功能

童欣; 刘地川; 吴泓权; 蔡敏

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超声微泡介导H-FABP基因改善慢性心衰大鼠的心功能

论著 | 更新时间：2026-01-09

- 超声微泡介导H-FABP基因改善慢性心衰大鼠的心功能
- Ultrasound microbubble-mediated heart fatty acid binding protein in treatment of chronic heart failure rats
- 陆军军医大学学报 2012年34卷第5期页码：396-400
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  中图分类号： R541.610.5;R445.1;R459.9
- 纸质出版：2012
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童欣,刘地川,吴泓权,蔡敏.超声微泡介导H-FABP基因改善慢性心衰大鼠的心功能[J].陆军军医大学学报(原第三军医大学学报),2012,34(05):396-400.

　Tong Xin,Liu Dichuan,Wu Hongquan,Cai Min.Ultrasound microbubble-mediated heart fatty acid binding protein in treatment of chronic heart failure rats[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(05):396-400.
童欣,刘地川,吴泓权,蔡敏.超声微泡介导H-FABP基因改善慢性心衰大鼠的心功能[J].陆军军医大学学报(原第三军医大学学报),2012,34(05):396-400. DOI：

　Tong Xin,Liu Dichuan,Wu Hongquan,Cai Min.Ultrasound microbubble-mediated heart fatty acid binding protein in treatment of chronic heart failure rats[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(05):396-400. DOI：

摘要

目的研究超声靶向破坏微泡（ultrasound targeted microbubble destruction，UTMD）技术转染H-FABP基因对心肌梗死后心功能的影响。方法通过结扎成年雄性Wistar大鼠46只，体质量（220±20）g，冠状动脉前降支建立心肌梗死模型。于心肌梗死8周后，将存活的31只心衰大鼠随机分为4组：①H-FABP+超声+微泡组（H-FABP+US/MB组，n=8），用超声破坏携H-FABP基因微泡转染大鼠心肌；②超声+微泡组（US/MB组，n=8），用超声破坏不含基因的微泡；③H-FABP+生理盐水组（H-FABP+NS组，n=8），由颈静脉输入含基因的生理盐水；④单纯手术组（SA组，n=7），仅由颈静脉输入生理盐水；⑤假手术组（SS组，n=6）。基因转染14 d后测定各组大鼠心功能，Western blot检测左心室非梗死区H-FABP表达，ELISA法检测静脉血及非梗死区心肌游离脂肪酸（FFA）含量，硫代巴比妥酸反应物（TBARS）法检测非梗死区心肌组织脂质过氧化水平，免疫组织化学法检测非梗死区心肌诱导型一氧化氮合酶（iNOS）表达。结果心肌梗死大鼠各组与假手术组比较心功能明显下降（P0.05），H-FABP表达明显下降（P0.05），静脉血及心肌FFA含量明显升高（P0.05），丙二醛（MDA）水平明显升高（P0.05），iNOS表达明显升高（P0.05）。H-FABP+超声+微泡组与心肌梗死大鼠中的另外3组比较心功能明显改善（P0.05），H-FABP表达升高（P0.05），心肌FFA含量降低（P0.05），MDA水平降低（P0.05），iNOS表达受抑制（P0.05）。结论超声微泡介导的H-FABP转染可改善大鼠慢性心衰时心功能。可能与通过提高H-FABP表达、降低心肌FFA含量、改善心肌氧化应激水平、进而抑制iNOS的表达有关。

Abstract

Objective To determine the effect of heart fatty acid binding protein (H-FABP) transfected by ultrasound targeted microbubble destruction (UTMD) technology on cardiac function after post-infarction. Methods Myocardial infarction (MI) was induced in Wistar male rats (n=46

220±20 g) by ligating the left anterior descending coronary artery. After 8 weeks

the 31 surviving rats with heart failure were randomly divided into 4 groups

H-FABP+ultrasound+microbubble group (H-FABP+US/MB group

n=8

ultrasound-targeted destruction microbubble loaded with H-FABP gene was transfected to rat heart)

ultrasound+microbubble group (US/MB group

n=8

ultrasonic destruction of microbubbles loaded without gene)

H-FABP+normal saline group (H-FABP+NS group

n=8

normal saline containing gene were infused from jugular vein)

surgery alone group (SA group

n=7

only normal saline were infused from jugular vein)

and sham-operation group (SS group

n=6). In 14 d after transfection

the cardiac function of all the rats were measured

H-FABP expression in non-infarct region of left ventricular was detected by Western blotting

free fatty acid (FFA) content of venous blood and non-infarct region myocardium were detected by ELISA

lipid peroxidation in non-infarct region of left ventricular was detected by thiobarbituric acid reactive substances (TBARS) method

and the iNOS expression in non-infarct region of left ventricular was detected by immunohistochemical assay. Results Compared with sham-operation group

left ventricular ejection fraction (LVEF) and the H-FABP expression were decreased significantly (P0.05)

free fatty acid content and malondialdehyde (MDA) level and the iNOS expression were obviously increased (P0.05) in the MI groups. Compared with US/MB

H-FABP+NS and SA groups

LVEF and the H-FABP expression were apparently increased (P0.05)

free fatty acid content of myocardium and MDA level were obviously decreased (P0.05) and the iNOS expression was markedly inhibited (P0.05) in H-FABP+US/MB group. Conclusion Ultrasound microbubble-mediated H-FABP transfection improves cardiac function via upregulating H-FABP

redu-cing myocardial FFA

ameliorating myocardial oxidative stress and inhibiting iNOS expression.

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