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抗菌肽 SR-0379 可刺激人内皮祖细胞修复外周动脉疾病。

The anti-microbial peptide SR-0379 stimulates human endothelial progenitor cell-mediated repair of peripheral artery diseases.

机构信息

Departments of Physiology, Pusan National University, Yangsan 50612, Korea.

Obstetrics and Gynecology, School of Medicine, Pusan National University, Yangsan 50612, Korea.

出版信息

BMB Rep. 2017 Oct;50(10):504-509. doi: 10.5483/bmbrep.2017.50.10.043.

DOI:10.5483/bmbrep.2017.50.10.043
PMID:28539159
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5683819/
Abstract

Ischemia is a serious disease, characterized by an inadequate blood supply to an organ or part of the body. In the present study, we evaluated the effects of the anti-microbial peptide SR-0379 on the stem cell-mediated therapy of ischemic diseases. The migratory and tube-forming abilities of human endothelial progenitor cells (EPCs) were enhanced by treatment with SR-0379 in vitro. Intramuscular administration of SR-0379 into a murine ischemic hindlimb significantly enhanced blood perfusion, decreased tissue necrosis, and increased the number of blood vessels in the ischemic muscle. Moreover, co-administration of SR-0379 with EPCs stimulated blood perfusion in an ischemic hindlimb more than intramuscular injection with either SR-0379 or EPCs alone. This enhanced blood perfusion was accompanied by a significant increase in the number of CD31- and α-SMApositive blood vessels in ischemic hindlimb. These results suggest that SR-0379 is a potential drug candidate for potentiating EPC-mediated therapy of ischemic diseases. [BMB Reports 2017; 50(10): 504-509].

摘要

缺血是一种严重的疾病,其特征是器官或身体的一部分供血不足。在本研究中,我们评估了抗微生物肽 SR-0379 对缺血性疾病干细胞介导治疗的影响。SR-0379 在体外处理可增强人内皮祖细胞(EPC)的迁移和管状形成能力。将 SR-0379 肌肉内给药到小鼠缺血性后肢可显著增强血液灌注,减少组织坏死,并增加缺血肌肉中的血管数量。此外,与单独给予 SR-0379 或 EPCs 相比,SR-0379 与 EPCs 共同给药可刺激缺血后肢的血液灌注。这种增强的血液灌注伴随着缺血后肢中 CD31 和 α-SMA 阳性血管数量的显著增加。这些结果表明,SR-0379 是增强 EPC 介导的缺血性疾病治疗的潜在药物候选物。[BMB 报告 2017;50(10):504-509]。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edc9/5683819/c945c8ff0f54/bmb-50-504f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edc9/5683819/2f837efdf993/bmb-50-504f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edc9/5683819/6bdd1a5dfc92/bmb-50-504f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edc9/5683819/b9b90511970c/bmb-50-504f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edc9/5683819/c945c8ff0f54/bmb-50-504f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edc9/5683819/2f837efdf993/bmb-50-504f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edc9/5683819/6bdd1a5dfc92/bmb-50-504f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edc9/5683819/b9b90511970c/bmb-50-504f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edc9/5683819/c945c8ff0f54/bmb-50-504f4.jpg

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本文引用的文献

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