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首页> 外文期刊>Circulation journal >Donepezil Can Improve Ischemic Muscle Atrophy by Activating Angiomyogenic Properties of Satellite Cells
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Donepezil Can Improve Ischemic Muscle Atrophy by Activating Angiomyogenic Properties of Satellite Cells

机译：Denpezil可以通过激活卫星细胞的血管生成特性来改善缺血性肌肉萎缩

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Background: Saving more limbs of patients with peripheral arterial disease (PAD) from amputation by accelerating angiogenesis in affected limbs has been anticipated for years. We hypothesized that an anti-Alzheimer drug, donepezil (DPZ), can activate angiomyogenic properties of satellite cells, myogenic progenitors, and thus be an additional pharmacological therapy against PAD. Methods?and?Results: In a murine hindlimb ischemia model, we investigated the angiogenic effects of a clinical dose of DPZ (0.2 mg·kg–1·day–1) and its combination with cilostazol, a platelet aggregation inhibitor and a conventional therapeutic drug against PAD. The combination therapy most effectively improved skin coldness and most effectively upregulated vascular endothelial growth factor (VEGF)-producing satellite cells in ischemic hindlimbs. Computed tomography revealed that DPZ remarkably attenuated ischemic muscle atrophy and induced super-restoration in affected hindlimbs. The in vitro study with human aortic endothelial cells showed that DPZ or its combination with cilostazol effectively upregulated the expression of pAkt, hypoxia inducible factor-1α, and VEGF protein. Likewise, in primary cultured satellite cells, DPZ, alone or in combination, upregulated the expression of VEGF, interleukin-1β, and fibroblast growth factor 2 protein. Conclusions: The present results suggest that a clinical dosage of DPZ accelerates angiomyogenesis by directly acting on both endothelial and satellite cells. Therefore, DPZ is a potential additional choice for conventional drug therapy against PAD. ( Circ J 2014; 78: 2317–2324)
机译：背景：通过加速受影响的肢体中的血管生成，预计将在截肢中拯救更多患者患有周围动脉疾病（垫）的患者。我们假设抗阿尔茨海默药物，DepPezil（DPZ），可以激活卫星细胞，肌原血管血管发射器的血管生成特性，因此是对垫的额外药理学疗法。方法？结果：在鼠后肢缺血模型中，我们研究了DPZ临床剂量的血管生成效应（0.2mg·kg -1天 -1·stay -1/4）及其与西洛司唑，血小板聚集抑制剂和常规治疗药物的联合。联合疗法最有效地改善了皮肤寒冷，最有效地上调的血管内皮生长因子（VEGF） - 缺血性后肢的卫星细胞。计算机断层摄影显示DPZ显着减弱缺血性肌肉萎缩，并在受影响的后肢诱导超恢复。与人主动脉内皮细胞的体外研究表明，DPZ或其与西洛司唑的组合有效地上调了PAKT，缺氧诱导因子-1α和VEGF蛋白的表达。同样，在初级培养的卫星细胞中，DPZ，单独或组合，上调VEGF，白细胞介素-1β和成纤维细胞生长因子2蛋白的表达。结论：本结果表明，DPZ的临床剂量通过直接作用于内皮和卫星细胞来加速血管生成。因此，DPZ是对垫的常规药物治疗的潜在额外选择。 （2014年CIRC; 78：2317-2324）

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