Abstract��OBJECTIVE To investigate the influence and mechanism of different doses of Yangxinshi on infarction region angiogenesis of Wistar rats after acute myocardial infarction. METHODS Sixty healthy male Wistar rats were randomly divided into five groups, named as follow:group A: rosuvastatin group (0.75 mg��kg-1��d-1), group B: high-dose Yangxinshi(0.27 g��kg-1��d-1),group C:mid-dose Yangxinshi group (0.18 g��kg-1��d-1),group D: Low-dose Yangxinshi group (0.09 g��kg-1��d-1),group E:saline control group. A, B, C, D group was respectively given the drug by gavage, group E received normal saline by gavage. The models of acute myocardial infarction can be established in the forth week . After continued drugs for 4 weeks, rats were killed before detected blood biochemicalindexes such as blood lipids, liver and kidney function. Myocardial tissue was sliced and stained infarcted myocardium by HE to observe the pathological changes, also extract ischemic and infarct myocardium tissue protein and test VEGF protein expression with immunohistochemistry. RESULTS Myocardial tissue HE staining were observed a lot of survival island cardiomyocytes and neonatal thin-walled capillaries in four treatment groups , however,control group exist less normal cardiomyocytes and capillaries mainly disappear. Immunohistochemistry RESULTS showed high-doses of Yangxinshi group express higher VEGF protein compared with mid-dose group, low-dose group and control group, the difference was statistically significant (P<0.05), VEGF protein expression was significantly increased the in mid-dose and high-dose Yangxinshi groups than rosuvastatin group, the difference was statistically significant (P<0.05). CONCLUSION Yangxinshi promote production of VEGF protein and angiogenesis of ischemic myocardium ,in addition its role and its dose is positive correlated. VEGF protein expression was significantly increased the in mid-dose and high-dose Yangxinshi groups than rosuvastatin group, the difference is statistically significant (P<0.05).
��ѩ��, ����, �Ž���, ��Т��, ֣��, ���Ʒ�. ������Ƭ�ڼ����ļ���������Ѫ�������е����ü������о�[J]. �й�ҩѧ��־, 2016, 51(24): 2163-2168.
ZHANG Xue-juan, HAN Di, ZHANG Jie-tao, GUO Xiao-zi, ZHENG Yu, LI Yun-fa. The Impact and Mechanism of Different Doses of Yangxinshi on Cardiac Angiogenesis of Acute Myocardial Infarction in Rats. Chinese Pharmaceutical Journal, 2016, 51(24): 2163-2168.
SAGER P T, MELAN I L, LIPKA L, et al. Effect of coadministration of ezetimibe and simvastatin on high-sensitivity C-reactive protein[J]. Am J Cardiol, 2003, 92(12):1414-1418.
[2]
YIN N, CHEN S X, LUO W J, et al. Establishing the model of myocardial infarction by ligation of the left anterior desending branch in rats[J]. J Chin Phys (�й�ҽʦ��־),2006, 8(9):1193-1195.
[3]
WEI F, ZHANG J, HAN K, et al. Establishing a model of acute myocardial infarction in rats without artificial ventilation[J]. J Xi'an Jiaotong Univ(Med Sci)(������ͨ��ѧѧ��:ҽѧ��),2010, 29(6):699-702.
[4]
SYED I S, SANBORN T A, ROSENGART T K. Therapeutic angiogenesis: a biologic bypass[J]. Cardiology, 2004,101(1-3):131-143.
[5]
URBICH C, DEMBACH E, ZEIHER A M, et al.Double-edged role of statins in angiogenesis signaling[J].Circ Res,2002,90(6):737-744.
[6]
BANAI S, JAKLITSCH M T, SHOU M, et al. Angiogenic-induced enhaIlcement of collateral blood now to ischemic myocardium by vacular endothelial growth factor in dogs[J]. Circulation, 1994, 89(5):2183-2189.
[7]
LAVINE K J, ORNITZ D M.Rebuilding the coronary vasculature:hedgehog as a new candidate for pharmacologic revascul-arization[J]. Trends Cardiovasc Med, 2007, 17(3):77-83.
[8]
HUANG P, LIU C Y, XU X Y, et al. The effect of high intensity laser beam on the biological regulation of monolayer skin fibroblasts[J]. Chin Laser(�����), 2005, 32(5):723-728.
[9]
LI X I, WANG Z G, LING Z Y, et al. Stimulation of myocardial angiogenesis by ultrasound-mediated microbubble destruction in rats[J]. Chin J Ultrasound Med(�й�����ҽѧ��־),2007, 23(1):6-8.
[10]
EJIRI M, BEZOS A, TAINSKY M A. Effects of heparin treatment on collateraldevelopment and regional myocardial function in acute myocardialin farction [J].Am Heart J, 1990, 119(2 pt 1):248.
[11]
PICANO E, MICHELASSII C. Chronic oral dipyridamole as anovel antianginal drug:the collateral hypothesis [J]. Cardiovasc Res, 1997, 33 (3):666-670.
[12]
ZHANG J J, ZHANG A B, CHEN S Y, et al. The polysaccharide sulfate enhance neovascularization of acidic fibroblast growth factor[J]. Chin J Cardiov(�й���Ѫ����־),1997, 2(1):12.
[13]
ASSMUS B, URBICH C, AICHER A, et al. HMG-CoA reductase inhibitors reduce senescence and increase proliferation of endothelial progenitor cellsviaregulation of cell cycle regulatory genes[J]. Circ Res, 2003, 92(9):1049-1055.
[14]
URBICH C, DEMBACH E, ZEIHER A M, et al. Double-edged role of statins in angiogenesis signaling[J]. Circ Res, 2002, 90(6):737-744.
[15]
ZENG J B. Advances in vascular endothelial growth factor[J]. Foreign Med(Mol Biol Sec)(����ҽѧ:��������ѧ�ֲ�), 2000, 22(1):87-92.
[16]
JACKSON K, MAJKA M, WANG H. et al. Regeneration of ischemic cardiac muscle and vascular endothelium by adult stemcells[J]. J Clin Invest, 2001, 107(11):1395-1402.
[17]
LI C Y,HE X Q, YU J H. Discussion on the mechanism of the clinical application of Yangxinshi tablets[J]. Chin J Geriatric Health Care(�й����걣��ҽѧ��־), 2010,8(4):79-80.
2016, Vol. 51 
