Effects of Astragaloside IV on heart failure in rats

被引:50
作者
Zhao Z. [1 ]
Wang W. [1 ]
Wang F. [2 ]
Zhao K. [3 ]
Han Y. [1 ]
Xu W. [1 ]
Tang L. [1 ]
机构
[1] State Key Laboratory of Pharmacokinetics and Pharmacodynamics, Tianjin Institute of Pharmaceutical Research
[2] Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology
[3] Department of Pharmacy, Tianjin Medical College
关键词
Left Ventricle; Model Group; Infarcted Area; Quinapril; Fractional Shorten;
D O I
10.1186/1749-8546-4-6
中图分类号
学科分类号
摘要
Background: Astragaloside IV (ASI) in Radix Astragali is believed to be the active component in treating heart failure. The present study aims to examine the effects of ASI on cardiovascular parameters in long-term heart failure in rats. Methods: Using echocardiographic and haemodynamic measurements, we studied the effects of ASI on congestive heart failure (CHF) induced by ligation of the left coronary artery in rats. Results: ASI (0.1, 0.3 and 1.0 mg/kg/day) attenuated the decline of fractional shortening (FS). The peak derivatives of the left ventricle (LV) pressure (dp/dt) in ASI-treated groups significantly increased. Both LV internal diameters in diastole (LVIDd) and in systole (LVIDs) decreased significantly after ASI treatment (0.3 and 1.0 mg/kg/day). ASI (1.0 mg/kg/day) attenuated the decrease of LV systolic pressure (LVSP). ASI treatment inhibited compensatory hypertrophy of myocardial cells and lowered the number of apoptotic myocytes. Conclusion: ASI improved cardiac functions as measured by cardiovascular parameters. © 2009 Zhao et al; licensee BioMed Central Ltd.
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共 30 条
[11]  
Luo H.M., Dai R.H., Li Y., Shi H.M., Guan Y.H., Gong Z.M., Liu X.J., Nuclear cardiology study on effective ingredients of austragalus membranaceus in treating heart failure, Zhongguo Zhongxiyi Jiehe Zazhi, 15, 12, pp. 707-709, (1995)
[12]  
Zhang Z.C., Li S.J., Yang Y.Z., Chen R.Z., Ge J.B., Chen H.Z., Effect of astragaloside on cardiomyocyte apoptosis in murine coxsackievirus B3 myocarditis, J Asian Nat Prod Res, 9, 2, pp. 145-151, (2007)
[13]  
Vscovo G., Volterrani M., Zennaro R., Apoptosis in the skeletal muscle of patients with heart failure: Investigation of clinical and biochemical changes, Heart, 84, pp. 431-437, (2000)
[14]  
Libera L.D., Ravara B., Angelini A., Rossini K., Sandri M., Thiene G., Benificial effects on skeletal muscle of the angiotension II type 1 receptor blocker irbesartan in experimental heart failure, Circulation, 103, pp. 2195-2200, (2001)
[15]  
Khoynezhad A., Jalali Z., Tortolani A.J., A Synopsis of Research in Cardiac Apoptosis and Its Application to Congestive Heart Failure, Tex Heart Inst J, 34, 3, pp. 352-359, (2007)
[16]  
Narila J., Haider N., Virmani R., Apoptosis in myocytes in end stage heart failure, N Engl J Med, 335, pp. 1182-1189, (1996)
[17]  
Tonnessen T., Christensen G., Oie E., Holt E., Kjekshus H., Smiseth O.A., Sejersted O.M., Attramadal H., Increased cardiac expression of endothelin-1 mRNA in ischemic heart failure in rats, Cardiovasc Res, 33, pp. 601-610, (1997)
[18]  
Burrell L.M., Chan R., Phillips P.A., Validation of an echocardiographic assessment of cardiac function following moderate size myocardial infarction in the rat, Clin Exp Pharmacol Physiol, 23, 6, pp. 570-572, (1996)
[19]  
Francis G.S., Pathophysiology of chronic heart failure, Am J Med, 110, SUPPL. 7A, pp. 37-46, (2001)
[20]  
Ahmet I., Krawczyk M., Heller P., Beneficial effects of chronic pharmacological manipulation of β-adrenoreceptor subtype signaling in rodent dilated ischemic cardiomyopathy, Circulation, 110, 9, pp. 1083-1090, (2004)