粒细胞集落刺激因子作为大鼠糖尿病神经病变的一种治疗方法。

Granulocyte-colony stimulating factor as a treatment for diabetic neuropathy in rat.

作者信息

Kim Kyung-Soo, Song Yi-Sun, Jin Jiyong, Joe Jun-Ho, So Byung-Im, Park Jun-Young, Fang Cheng-Hu, Kim Mi Jung, Cho Youl-Hee, Hwang Sejin, Ro Young-Suck, Kim Hyuck, Ahn You-Hern, Sung Hak-Joon, Sung Jung-Joon, Park Sung-Hye, Lipton Stuart A

机构信息

Division of Cardiology, Hanyang University College of Medicine, Seoul, 133-792, South Korea; Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, 133-792, South Korea.

Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, 133-792, South Korea.

出版信息

Mol Cell Endocrinol. 2015 Oct 15;414:64-72. doi: 10.1016/j.mce.2015.07.014. Epub 2015 Jul 17.

DOI:10.1016/j.mce.2015.07.014

PMID:26190836

Abstract

Effective treatment of diabetic neuropathy (DN) remains unsolved. We serendipitously observed dramatic relief of pain in several patients with painful DN receiving granulocyte-colony stimulating factor (G-CSF). The aim of this study was to determine if G-CSF could treat DN in an animal model and to ascertain its mechanism of action. In a rodent model of DN, G-CSF dramatically recovered nerve function, retarded histological nerve changes and increased the expression of neurotrophic factors within nerve. A sex-mismatched bone marrow transplantation (BMT) study revealed that G-CSF treatment increased the abundance of bone marrow (BM)-derived cells in nerves damaged by DN. However, we did not observe evidence of transdifferentiation or cell fusion of BM-derived cells. The beneficial effects of G-CSF were dependent on the integrity of BM. In conclusion, G-CSF produced a therapeutic effect in a rodent model of DN, which was attributed, at least in part, to the actions of BM-derived cells.

摘要

糖尿病神经病变（DN）的有效治疗方法仍未找到。我们意外地观察到，几名接受粒细胞集落刺激因子（G-CSF）治疗的疼痛性DN患者的疼痛得到了显著缓解。本研究的目的是确定G-CSF是否能在动物模型中治疗DN，并确定其作用机制。在DN的啮齿动物模型中，G-CSF显著恢复了神经功能，延缓了神经组织学变化，并增加了神经内神经营养因子的表达。一项性别不匹配的骨髓移植（BMT）研究表明，G-CSF治疗增加了DN损伤神经中骨髓（BM）来源细胞的数量。然而，我们没有观察到BM来源细胞转分化或细胞融合的证据。G-CSF的有益作用依赖于BM的完整性。总之，G-CSF在DN的啮齿动物模型中产生了治疗效果，这至少部分归因于BM来源细胞的作用。