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胰岛素诱导低血糖性神经病变中的自噬作用。

Autophagy in insulin-induced hypoglycaemic neuropathy.

机构信息

Division of Cell Biology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden.

出版信息

Pathology. 2011 Apr;43(3):254-60. doi: 10.1097/PAT.0b013e328343c992.

Abstract

AIM

Autophagy in neurons has been linked to a growing number of pathological conditions in the CNS, but the role of this process in peripheral neuropathy has received little attention. This study aimed to determine whether autophagy is involved in development of peripheral neuropathy in hypoglycaemic diabetic rats.

METHODS

The lateral plantar nerves, ventral roots, and dorsal roots of insulin-treated diabetic hypoglycaemic rats were examined for structural signs of autophagy by electron microscopy.

RESULTS

Autophagy-associated vacuoles were found in myelinated axons exhibiting early pathological changes but not in the associated Schwann cells. When the damaged axons degenerated, their associated Schwann cells gradually died and were cleared from the endoneurium by macrophages. During axonal regeneration, extensive signs of autophagy-related structures such as autophagophores appeared in regenerating axons and in the cytoplasm of the associated Schwann cells in the Band of Büngner.

CONCLUSION

Autophagy occurs in hypoglycaemic peripheral nerves in association with axonal de- and regeneration. The extensive signs of autophagy in regenerated axons suggest that autophagy may play a role in survival of the new axons.

摘要

目的

神经元自噬与中枢神经系统(CNS)越来越多的病理状况有关,但这一过程在周围神经病变中的作用却很少受到关注。本研究旨在确定自噬是否参与了低血糖糖尿病大鼠周围神经病变的发生。

方法

通过电子显微镜检查胰岛素治疗的糖尿病低血糖大鼠的足底外侧神经、腹根和背根,以观察自噬的结构特征。

结果

在表现出早期病理变化的有髓轴突中发现了与自噬相关的空泡,但在相关的施万细胞中没有发现。当受损的轴突退化时,其相关的施万细胞逐渐死亡,并被巨噬细胞从神经内膜中清除。在轴突再生过程中,大量与自噬相关的结构,如自噬体,出现在再生轴突和邦格氏带中相关施万细胞的细胞质中。

结论

自噬发生在低血糖性周围神经中,与轴突的去再生有关。再生轴突中广泛存在的自噬迹象表明,自噬可能在新轴突的存活中发挥作用。

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