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单核细胞趋化因子-1在等长收缩运动促进大鼠缺血心肌侧支动脉生成中的作用 被引量:1

Effects of MCP-1 in isometric exercise training promotes the collateral artery formation in mice with myocardial ischemia
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摘要 目的:探讨单核细胞趋化因子-1(MCP-1)在等长收缩运动训练促进缺血心肌侧支动脉生成中的作用。方法:将造模成功的24只雄性SD大鼠,体重(200±20)g,随机分为4组:对照组(CG)、心肌缺血组(MI)、运动训练组(ET)、MCP-1抑制剂组(LG),每组均有6只大鼠。CG组连续2周皮下注射生理盐水;MI组连续2周皮下注射异丙肾上腺素(10mg/kg/d),造成心肌缺血;ET组连续2周皮下注射异丙肾上腺素并且进行等长收缩运动训练;LG组在ET组的基础上进行MCP-1抑制剂来氟米特灌胃。训练8周结束后,麻醉大鼠,取左心室心肌,采用微球法测定缺血区心肌相对侧支循环血流量(RCBF);采用免疫组化法测定缺血区心肌小动脉密度和单核细胞数量;以Western blot和荧光定量PCR法测定缺血心肌中MCP-1的蛋白及mRNA的表达。结果:ET组大鼠的相对侧支血流量(RCBF)、小动脉密度(AD)明显高于其余3组(P<0.001),LG组的RCBF和AD与MI组相比无显著性差异;ET组大鼠缺血心肌中单核细胞数量、MCP-1 mRNA以及MCP-1蛋白表达均显著高于其余各组(P<0.001),而LG组大鼠缺血心肌中单核细胞数量、MCP-1 mRNA以及MCP-1蛋白表达与MI组相比无显著性差异。结论:持续8周的等长收缩运动训练可以增加大鼠缺血心肌中MCP-1的表达,从而促进缺血心肌侧支动脉的生成。 Objective: To investigate the role of monocyte chemoattractant protein-1 in the progress that isometric exercise training improves arteriogenesis. Method: Twenty-four male Sprague-Dawley rats were used, weighing (200-20)g. The rats were randomized in- to control group (CG), myocardial ischemia group (MI), exercise training group (ET), MCP-1 inhibitor group (LG). There were 6 rats in each group. Rats were continuously administered 10mg/kg subcutaneously isoprotere- nol for successive 2 weeks to establish the myocardial ischemia model. Successfully modeled rats were in groups MI, ET and LG. Isometric exercise training were performed in group ET and LG. The rats in group LG were given MCP-1 inhibitor leflunomide by gavage. After 8 weeks of training, the left ventricular myocar- dium was extracted and relative collateral blood flow (RCBF) was measured by microspheres. Artery density (AD) and monocytes were measured by immunohistochemistry analysis. Western blot analysis and real-time quantitative PCR were performed to assay protein and mRNA of MCP-1. Result: RCBF and AD increased significantly in group ET as compared to the rest groups. RCBF and AD in group LG showed higher than that in group MI but not significant. The number of monocytes, MCP-I mRNA and MCP-I expression were significantly elevated in ischemie myocardium of group ET. Interestingly, the num- ber of monocytes, MCP-1 mRNA and MCP-I expression showed lower than that in group MI but also not sig- nificant. Conclusion: Eight weeks of isometric exercise training can increase the expression of MCP-1 in ischemic myo- cardium and promote the arteriogenesis.
作者 管骏涛 耿灿茹 陆晓 GUAN Juntao GENG Canru LU Xiao(Rehabilitation Department, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029)
出处 《中国康复医学杂志》 CAS CSCD 北大核心 2017年第8期856-862,共7页 Chinese Journal of Rehabilitation Medicine
基金 国家自然科学基金资助项目(81472164)
关键词 等长收缩运动 心肌缺血 单核细胞趋化因子 侧支动脉生成 动脉密度 isometric exercise training myocardial ischemia monocyte chemoattractant protein arteriogenesis artery density
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  • 1励建安,赵伟英,周士枋,陆晓,张勤.Relationship between isometric exercise and myocardial ischemia in patients with coronary artery disease: an Echo- Doppler study[J].Chinese Medical Journal,2000(6):13-17. 被引量:3
  • 2刘元标,励建安,路鹏,王骏,金挺剑.家兔短暂心肌缺血后VEGF蛋白表达的空间规律[J].中国康复医学杂志,2004,19(6):422-425. 被引量:12
  • 3路鹏,励建安,刘元标,金挺剑,王骏.心肌短暂缺血后血管内皮生长因子表达的时间规律[J].中华物理医学与康复杂志,2004,26(10):577-580. 被引量:11
  • 4王战建,刘珊.糖尿病肾病发病机制的研究进展[J].国际泌尿系统杂志,2006,26(5):693-696. 被引量:41
  • 5陈俊抛 林煜 陈俊抛 林煜 主编.缺氧性脑病[A].陈俊抛,林煜,主编.痴呆治疗学:新理论、新观点、新技术[M].北京:人民军医出版社,2002.273-7.
  • 6Riedel BJ, Gal J, Ellis G,et al. Myocardial protection using fructose-1,6-diphosphate during coronary artery bypass graft surgery: a randomized, placebo-controlled clinical trial.A nesth A nalg 2004;98(1 ):20-9.
  • 7Karaca M, Kilic E, Yazici B,et al. Ischemic stroke in elderly patients treated with a free radical scavenger-glycolytic intermediate solution: a preliminary pilot trial. Neurol Res 2002;24(1):73-80.
  • 8Espanol MT, Litt L, Hasegawa K, et al. Fructoso-1,6-bisphosphate preserves adenosine triphosphate but not intracellular pH during hypoxia in respiring neonatal rat brain slicos.Anesthesiology 1998;88(2):461-72.
  • 9Donohoe PH, Fahlman CS, Bickler PE, et al. Neuroprotection and intracellular Ca2+ modulation with fructose-1,6-bisphosphate during in vitro hypoxia-ischemia involves phospholipase C-dependent signaling. Brain Res 2001;917(2):158-66.
  • 10Cardenas A, Hurtado O, Leza JC, et al. Fructose-1,6-bisphosphate inhibits the expression of inducible nitric oxide synthase caused by oxygen-glucose deprivation through the inhibition of glutamate release in rat forebrain slices.Nunyn Schmiedebergs Arch Pharmacol 2000;362(3):208-12.

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