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本文引用的文献

1
Role and possible mechanisms of clenbuterol in enhancing reverse remodelling during mechanical unloading in murine heart failure.克伦特罗在小鼠心力衰竭机械卸载过程中增强逆向重塑的作用及可能机制
Cardiovasc Res. 2008 Mar 1;77(4):695-706. doi: 10.1093/cvr/cvm106. Epub 2008 Jan 4.
2
Catecholaminergic neurotransmitters regulate migration and repopulation of immature human CD34+ cells through Wnt signaling.儿茶酚胺能神经递质通过Wnt信号通路调节未成熟人类CD34+细胞的迁移和再增殖。
Nat Immunol. 2007 Oct;8(10):1123-31. doi: 10.1038/ni1509. Epub 2007 Sep 9.
3
Cardiac micro-computed tomography for morphological and functional phenotyping of muscle LIM protein null mice.心脏微计算机断层扫描用于肌肉LIM蛋白缺失小鼠的形态学和功能表型分析。
Mol Imaging. 2007 Jul-Aug;6(4):261-8.
4
Selective functional exhaustion of hematopoietic progenitor cells in the bone marrow of patients with postinfarction heart failure.心肌梗死后心力衰竭患者骨髓中造血祖细胞的选择性功能耗竭。
J Am Coll Cardiol. 2007 Jun 19;49(24):2341-9. doi: 10.1016/j.jacc.2007.01.095. Epub 2007 Jun 4.
5
Molecular signature of recovery following combination left ventricular assist device (LVAD) support and pharmacologic therapy.左心室辅助装置（LVAD）支持与药物治疗联合应用后恢复的分子特征。
Eur Heart J. 2007 Mar;28(5):613-27. doi: 10.1093/eurheartj/ehl365. Epub 2006 Nov 28.
6
Left ventricular assist device and drug therapy for the reversal of heart failure.左心室辅助装置与药物治疗用于心力衰竭的逆转
N Engl J Med. 2006 Nov 2;355(18):1873-84. doi: 10.1056/NEJMoa053063.
7
Effect of clenbuterol on cardiac and skeletal muscle function during left ventricular assist device support.克伦特罗对左心室辅助装置支持期间心脏和骨骼肌功能的影响。
J Heart Lung Transplant. 2006 Sep;25(9):1084-90. doi: 10.1016/j.healun.2006.06.017.
8
Comparison of relative mRNA quantification models and the impact of RNA integrity in quantitative real-time RT-PCR.相对mRNA定量模型的比较以及RNA完整性在实时定量RT-PCR中的影响
Biotechnol Lett. 2006 Oct;28(19):1601-13. doi: 10.1007/s10529-006-9127-2. Epub 2006 Aug 10.
9
Excitation-contraction coupling in the MLP knockout mouse.MLP基因敲除小鼠中的兴奋-收缩偶联
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慢性克仑特罗治疗调节心肌病小鼠模型中的内皮祖细胞和循环因子。

Chronic treatment with clenbuterol modulates endothelial progenitor cells and circulating factors in a murine model of cardiomyopathy.

机构信息

Lillehei Heart Institute, University of Minnesota, 312 Church Street, Minneapolis, MN 55455, USA.

出版信息

J Cardiovasc Transl Res. 2009 Jun;2(2):182-90. doi: 10.1007/s12265-009-9089-6. Epub 2009 Mar 27.

DOI:10.1007/s12265-009-9089-6
PMID:20559986
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4066445/
Abstract

The purpose of this study was to determine the effects of chronic treatment with the beta 2 adrenergic receptor agonist clenbuterol on endothelial progenitor cells (EPC) in a well-characterized model of heart failure, the muscle LIM protein knockout (MLP(-/-)) mouse. MLP(-/-) mice were treated daily with clenbuterol (2 mg/kg) or saline subcutaneously for 6 weeks. Clenbuterol led to a 30% increase in CD31(+) cells in the bone marrow of MLP(-/-) heart failure mice (p < 0.004). Clenbuterol did not improve ejection fraction. Clenbuterol treatment in MLP(-/-) mice was associated with significant changes in the following circulating factors: tissue inhibitor of metalloproteinase-type 1, leukemia inhibitory factor 1, C-reactive protein, apolipoprotein A1, fibroblast growth factor 2, serum glutamic oxaloacetic transaminase, macrophage-derived chemokine, and monocyte chemoattractant protein-3. Clenbuterol treatment in the MLP(-/-) model of heart failure did not rescue heart function, yet did increase CD31(+) cells in the bone marrow. This is the first evidence that a beta 2 agonist increases EPC proliferation in the bone marrow in a preclinical model of heart failure.

摘要

这项研究的目的是确定在心力衰竭的一种典型模型（即肌球蛋白结合蛋白 LIM 基因敲除（MLP(-/-)）鼠）中，长期使用β2 肾上腺素能受体激动剂克仑特罗（clenbuterol）治疗对内皮祖细胞（EPC）的影响。将 MLP(-/-) 小鼠每日皮下给予克仑特罗（2mg/kg）或生理盐水，治疗 6 周。克仑特罗导致 MLP(-/-)心力衰竭小鼠骨髓中 CD31(+)细胞增加 30%（p<0.004）。克仑特罗并未改善射血分数。克仑特罗治疗 MLP(-/-)小鼠与以下循环因子的显著变化相关：基质金属蛋白酶 1 型组织抑制剂、白血病抑制因子 1、C 反应蛋白、载脂蛋白 A1、成纤维细胞生长因子 2、血清谷氨酸草酰乙酸转氨酶、巨噬细胞衍生趋化因子和单核细胞趋化蛋白-3。在心力衰竭的 MLP(-/-)模型中，克仑特罗治疗并未挽救心功能，但确实增加了骨髓中的 CD31(+)细胞。这是首个证明β2 激动剂在心力衰竭的临床前模型中增加骨髓中 EPC 增殖的证据。