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J Reconstr Microsurg 2018; 34(07): 537-548
DOI: 10.1055/s-0038-1642023
Original Article
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Chronic Nerve Compression Accelerates the Progression of Diabetic Peripheral Neuropathy in a Rat Model: A Study of Gene Expression Profiling

Yiji Tu   *
1   Department of Orthopedics, Zhongshan Hospital, Fudan University, Shanghai, China
2   Joseph M. Still Burn and Reconstructive Center, Jackson, Mississippi
,
Zenggan Chen   *
1   Department of Orthopedics, Zhongshan Hospital, Fudan University, Shanghai, China
,
Junda Hu
1   Department of Orthopedics, Zhongshan Hospital, Fudan University, Shanghai, China
,
Zuoyou Ding
1   Department of Orthopedics, Zhongshan Hospital, Fudan University, Shanghai, China
,
William C. Lineaweaver
2   Joseph M. Still Burn and Reconstructive Center, Jackson, Mississippi
,
A. Lee Dellon
3   Department of Plastic Surgery, Johns Hopkins University, Baltimore, Maryland
,
Feng Zhang
1   Department of Orthopedics, Zhongshan Hospital, Fudan University, Shanghai, China
2   Joseph M. Still Burn and Reconstructive Center, Jackson, Mississippi
› Institutsangaben Funding This work was supported by a grant from the Recruitment Program of Global Experts in Fudan University (number: EZF152501).
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26. September 2017

06. März 2018

Publikationsdatum:
25. April 2018 (online)

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Abstract

Objective This article investigates the role of chronic nerve compression in the progression of diabetic peripheral neuropathy (DPN) by gene expression profiling.

Methods Chronic nerve compression was created in streptozotocin (STZ)-induced diabetic rats by wrapping a silicone tube around the sciatic nerve (SCN). Neurological deficits were evaluated using pain threshold test, motor nerve conduction velocity (MNCV), and histopathologic examination. Differentially expressed genes (DGEs) and metabolic processes associated with chronic nerve compression were analyzed.

Results Significant changes in withdrawal threshold and MNCV were observed in diabetic rats 6 weeks after diabetes induction, and in DPN rats 4 weeks after diabetes induction. Histopathologic examination of the SCN in DPN rats presented typical changes of myelin degeneration in DPN. Function analyses of DEGs demonstrated that biological processes related to inflammatory response, extracellular matrix component, and synaptic transmission were upregulated after diabetes induction, and chronic nerve compression further enhanced those changes. While processes related to lipid and glucose metabolism, response to insulin, and apoptosis regulation were inhibited after diabetes induction, chronic nerve compression further enhanced these inhibitions.

Conclusion Our study suggests that additional silicone tube wrapping on the SCN of rat with diabetes closely mimics the course and pathologic findings of human DPN. Further studies are needed to verify the effectiveness of this rat model of DPN and elucidate the roles of the individual genes in the progression of DPN.

Keywords

diabetes - peripheral neuropathy - DNA microarray

* Yiji Tu and Zenggan Chen contributed equally to the study and should be the co-first authors.