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首页> 中文期刊> 《中华医学杂志（英文版）》 >Tongxinluo Improves Apolipoprotein E-Deficient Mouse Heart Function

Tongxinluo Improves Apolipoprotein E-Deficient Mouse Heart Function

         
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摘要

Background:Our previous studies have shown that Tongxinluo (TXL),a compound Chinese medicine,can decrease myocardial ischemia-reperfusion injury,protect capillary endothelium function,and lessen cardiac ventricle reconstitution in animal models.The aim of this study was to illuminate whether TXL can improve hypercholesterolemia-impaired heart function by protecting artery endothelial function and increasing microvascular density (MVD) in heart.Furthermore,we will explore the underlying molecular mechanism of TXL cardiovascular protection.Methods:After intragastric administration of TXL (0.l ml/10 g body weight) to C57BL/6J wild-type mice (n =8) and ApoE-/-mice (n =8),total cholesterol,high-density lipoprotein-cholesterol,very-low-density lipoprotein (VLDL)-cholesterol,triglyceride,and blood glucose levels in serum were measured.The parameters of heart rate (HR),left ventricular diastolic end diameter,and left ventricular systolic end diameter were harvested by ultrasonic cardiogram.The left ventricular ejection fraction,stroke volume,cardiac output,and left ventricular fractional shortening were calculated.Meanwhile,aorta peak systolic flow velocity (PSV),end diastolic flow velocity,and mean flow velocity (MFV) were measured.The pulsatility index (PI) and resistant index were calculated in order to evaluate the vascular elasticity and resistance.The endothelium-dependent vasodilatation was evaluated by relaxation of aortic rings in response to acetylcholine.Westem blotting and real-time quantitative reverse transcription polymerase chain reaction were performed for protein and gene analyses of vascular endothelial growth factor (VEGF).Immunohistochemical detection was performed for myocardial CD34 expression.Data in this study were compared by one-way analysis of variance between groups.A value ofP ＜ 0.05 was considered statistically significant.Results:Although there was no significant decrease of cholesterol level (F =2.300,P =0.240),TXL inhibited the level of triglyceride and VLDL (F =9.209,P =0.024 and F =9.786,P =0.020,respectively) in ApoE-/-mice.TXL improved heart function of ApoE-/-mice owing to the elevations of LVEE SV,CO,and LVFS (all P ＜ 0.05).TXL enhanced aortic PSV and MFV (F =10.774,P =0.024 and F =11.354,P =0.020,respectively) and reduced PI of ApoE-/-mice (1.41 ± 0.17 vs.1.60 ± 0.17;P =0.037).After incubation with 10 μmol/L acetylcholine,the ApoE-/-mice treated with TXL aortic segment relaxed by 44％ ± 3％,significantly higher than control group mice (F =9.280,P =0.040).TXL also restrain the angiogenesis of ApoE-/-mice aorta (F =21.223,P =0.010).Compared with C57BL/6J mice,the MVD was decreased in heart tissue of untreated ApoE-/-mice (54.0 ± 3.0/mm2 vs.75.0 ± 2.0/mm2;F =16.054,P =0.010).However,TXL could significantly enhance MVD (65.0 ± 5.0/mm2 vs.54.0 ± 3.0/mm2;F =l 1.929,P =0.020) in treated ApoE-/-mice.In addition,TXL obviously increased the expression of VEGF protein determined by Western blot (F =20.247,P =0.004).Conclusions:TXL obviously improves the ApoE-/-mouse heart function from different pathways,including reduces blood fat to lessen atherosclerosis;enhances aortic impulsivity,blood supply capacity,and vessel elasticity;improves endothelium-dependent vasodilatation;restraines angiogenesis of aorta-contained plaque;and enhances MVD of heart.The molecular mechanism of MVD enhancement maybe relate with increased VEGF expression.

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  • 来源
    《中华医学杂志（英文版）》 |2018年第5期|544-552|共9页
  • 作者

    Guo-Qiang Yuan; Song Gao; Yong-Jian Geng; Yao-Ping Tang; Min-Juan Zheng; Harnath S Shelat; Scott Collins; Han-Jing Wu; Yi-Ling Wu;

  • 作者单位

    Department of Collateral Disease, Research Institute of Integrated Traditional Chinese Medicine and Western Medicine of Hebei, Shijiazhuang,Hebei 050035, China;

    Department of Cardiovascular Disease, Hebei Yiling Hospital, Shijiazhuang, Hebei 050091, China;

    Department of Internal Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, PX 77030, USA;

    Department of Internal Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, PX 77030, USA;

    Center for Cell Signaling, Institute of Molecular Medicine, Houston Health Science Center, The University of TX, Houston, TX 77030, USA;

    Department of Pediatric Cardiology, Baylor College of Medicine, Houston, TX 77030, USA;

    Department of Internal Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, PX 77030, USA;

    Department of Internal Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, PX 77030, USA;

    Department of Internal Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, PX 77030, USA;

    Department of Collateral Disease, Research Institute of Integrated Traditional Chinese Medicine and Western Medicine of Hebei, Shijiazhuang,Hebei 050035, China;

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