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加参方对急性心肌梗死模型大鼠心肌组织单核-巨噬细胞及血管细胞黏附分子1表达的影响 被引量:3

Effects of Jiashen Fang (加参方) on the Expression of Myocardial Tissue Monocyte-Macrophage and Vascular Cell Adhesion Molecule-1 in Rats Model of Acute Myocardial Infarction
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摘要 目的探讨加参方对心肌梗死大鼠心功能的影响及可能作用机制。方法采用结扎大鼠左冠状动脉前降支的方法建立大鼠急性心肌梗死模型,将术后24 h成活大鼠随机分为假手术组(19只)、模型组(30只)、加参方低剂量组(31只)、加参方高剂量组(30只)和氯沙坦组(30只)。加参方低、高剂量组分别给予加参方浸膏含生药量3、6 g/(kg·d),氯沙坦组给予氯沙坦片10 mg/(kg·d),假手术组和模型组给予相同体积蒸馏水,各组连续灌胃4周。分别于给药后1、4周末超声检测心功能,测定心肌组织缺血危险区单核-巨噬细胞计数及血管细胞黏附分子-1(VCAM-1)蛋白表达量。结果与假手术组同时间点比较,模型组大鼠心功能降低,心肌组织中单核-巨噬细胞计数及VCAM-1蛋白表达显著升高(P<0.05);与模型组同时间点比较,氯沙坦组和加参方高剂量组大鼠心功能改善明显,心肌组织单核-巨噬细胞计数和VCAM-1表达降低(P<0.05)。结论加参方可能通过抑制大鼠心肌组织单核-巨噬细胞的浸润及VCAM-1蛋白表达,从而改善心室重构,提高心功能。 Objective To study the effects of Jiashen Fang( 加参方) on the cardiac function of rats with myocardial infarction and to explore the possible mechanism. Methods Anterior descending branch of left coronary artery of rats were ligatured to establish the rat models of acute myocardial infarction. Twenty-four hours after the operation,the survival rats were randomly divided into a control group( 19),a model group( 30),a low dose of Jiashen Fang group( 31),a high dose of Jiashen Fang group( 30),and a losartan group( 30). The low and high dose of Jiashen Fang groups were given extractum of Jiashen Fang with 3 g /( kg·d) and 6 g /( kg·d) of pure dose,respectively. The losartan group was given 10 mg /( kg·d) of losartan tablets. The control group and the model group were given the equivalent distilled water. Each group was given medication or water by gavage for 4 weeks. One week and4 weeks after treatment,cardiac function was evaluated with ultrasonic testing,and levels of monocyte-macrophage and expression levels of vascular cell adhesion molecule-1( VCAM-1) in danger area of myocardial tissue ischemia were tested,respectively. Results Compared with the control group at the same time point,cardiac function of rats decreased,and level of monocyte-macrophage and protein expression of VCAM-1 in myocardial tissue increased significantly in the model group( P〈0. 05); Compared with the model group at the same time point,cardiac function of rats improved significantly,and level of monocyte-macrophage and expression of VCAM-1 in the myocardial tissue decreased in the losartan group and the high dose of Jiashen Fang group( P〈0. 05). Conclusion Jiashen Fang may inhibit infiltration of monocyte-macrophage and protein expression of VCAM-1 in myocardial tissue of rats,improve the ventricular remodeling and improve cardiac function.
出处 《中医杂志》 CSCD 北大核心 2016年第12期1065-1068,共4页 Journal of Traditional Chinese Medicine
基金 国家自然科学基金(81173410) 河南省创新型科技团队(C20130050) 河南省高校科技创新团队支持计划(13IRTSTHN012)
关键词 急性心肌梗死 加参方 单核-巨噬细胞 血管细胞黏附分子-1 acute myocardial infarction Jiashen Fang(加参方) monocyte-macrophage vascular cell adhesion molecule-1
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参考文献7

  • 1NAHRENDORF M,PITTET MJ,SWIRSKI FK.Monocytes:protagonists of infarct inflammation and repair after myocardial infarction[J].Circulation,2010,121(22):2437-2445.
  • 2谢世阳,王幼平,李彬,刘卫红,王永霞,王贺,朱明军.加参方对大鼠心梗早期心功能及心肌炎症因子表达的影响[J].世界科学技术-中医药现代化,2014,16(10):2106-2111. 被引量:9
  • 3ANZAI T.Post-infarction inflammation and left ventricular remodeling:a double-edged sword[J].Circ J,2013,77(3):580-587.
  • 4FERNNDEZ-VELASCO M,GONZLEZ-RAMOS S,BOSCL.Involvement of monocytes/macrophages as key factors in the development and progression of cardiovascular diseases[J].Biochem J,2014,458(2):187-193.
  • 5FRANTZ S,HOFMANN U,FRACCAROLLO D,et al.Monocytes/macrophages prevent healing defects and left ventricular thrombus formation after myocardial infarction[J].FASEB J,2013,27(3):871-881.
  • 6COOK-MILLS JM,ME M,ABDALAVALENCIA H.Vascular cell adhesion molecule-1 expression and signaling during disease:regulation by reactive oxygen species and antioxidants[J].Antioxid Redox Signal,2011,15(6):1607-1638.
  • 7CHULUYAN HE,SCHALL TJ,YOSHIMURA T,et al.IL-1 activation of endothelium supports VLA-4(CD49d/CD29)-mediated monocyte transendothelial migration to C5a,MIP-1alpha,RANTES,and PAF but inhibits migration to MCP-1:a regulatory role for endotheliu M-derived MCP-1[J].J Leukoc Biol,1995,58(1):71-79.

二级参考文献16

  • 1王怡,郭志军,徐强,马晓艳.加参方对CHF大鼠肾脏水通道蛋白(AQP)mRNA表达的影响[J].天津中医药大学学报,2007,26(4):188-191. 被引量:11
  • 2Parish R C, Evans J D. Inflammation in chronic heart failure. Ann Pharmacother, 2008, 42(7):1002-1016.
  • 3Sun D, Huang J, Zhang Z, et al. Luteolin Limits infarct size and im- proves cardiac function after myocardium ischemia/reperfusion injury in diabetic rats. PLoS One, 2012, 7(3):e33491.
  • 4Tsutamoto T, Wada A, Ohnishi M, et al. Transcardiac increase in tumor necrosis factor-alpha and left ventricular end-diastolic volume in pa- tients with dilated cardiomyopathy. Eur J Heart Fail, 2004, 6(2):173- 180.
  • 5Gross G J, Baker J E, Hsu A, et al. Evidence for a role of opioids in epoxyeicosatrienoic acid-induced cardioprotection in rat hearts. Am J Physiol, 2010, 298(6):H2201-H2207.
  • 6Kido M, Du L, Sullivan C C, et al. Hypoxia-inducible factor 1-alpha reduces infarction and attenuates progression of cardiac dysfunc- tion after myocardial infarcton in the mouse. J Am Coll Cardiol, 2005, 46(11):2116-2124.
  • 7Nian M, Lee P, Khaper N, et al. Inflammatory cytokines and postmyo- cardial infarction remodeling. Circ Res, 2004, 94(12):1543-1553.
  • 8Martire A, Fernandez B, Buehler A, et al. Cardiac overexpression of monocyte chemoattractant protein-1 in transgenic mice mimics isch- emic preconditioning through SAPK/JNK1/2 activation. Cardiovasc Res, 2003, 57(2):523-534.
  • 9Haudek S B, Taffet G E, Schneider M D, et al. TNF provokes cardio- myocyte apoptosis and cardiac remodeling through activation of mul- tiple cell death pathways. J Clin Invest, 2007, 117(9):2692-2701.
  • 10Zhang J, Cheng X, Liao Y H, et al. Simvastatin regulates myocardial cytokines expression and improves ventricular remodeling in rats after acute myocardial infarction. Cardiovasc Drugs Ther, 2005, 19(1):13-21.

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