Abstract

Spinal cord injury (SCI) induces complex biochemical changes, which result in inhibition of nervous tissue regeneration abilities. In this study, Fourier-transform infrared (FT-IR) spectroscopy was applied to assess the outcomes of implants made of a novel type of non-functionalized soft calcium alginate hydrogel in a rat model of spinal cord hemisection (n = 28). Using FT-IR spectroscopic imaging, we evaluated the stability of the implants and the effects on morphology and biochemistry of the injured tissue one and six months after injury. A semi-quantitative evaluation of the distribution of lipids and collagen showed that alginate significantly reduced injury-induced demyelination of the contralateral white matter and fibrotic scarring in the chronic state after SCI. The spectral information enabled to detect and localize the alginate hydrogel at the lesion site and proved its long-term persistence in vivo. These findings demonstrate a positive impact of alginate hydrogel on recovery after SCI and prove FT-IR spectroscopic imaging as alternative method to evaluate and optimize future SCI repair strategies.

Highlights

  • In traumatic spinal cord injury (SCI) necrotic cell death and vascular damage take place at the lesion site immediately after the trauma

  • Degradation of contralateral white matter takes place in rat models at the chronic stage after hemisection, it includes demyelination and affects function. [42,43] Our findings suggest that the non-functionalized Ca2+-alginate hydrogel has a positive impact on presence of myelin in contralateral white matter

  • Instead of performing multiple immunohistochemical stainings on consecutive sections, this technique enables to address the different aspects of SCI in one dataset

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Summary

Introduction

In traumatic spinal cord injury (SCI) necrotic cell death and vascular damage take place at the lesion site immediately after the trauma. A cascade of secondary events including inflammation, edema and ischemia leads to additional cell death, demyelination and axonal degeneration, which culminate in further loss of nervous functions [1]. This cascade leads to the formation of a scar composed by reactive astrocytes, proteoglycans and extracellular matrix. In case of lacerating injury, a dense fibrous scar surrounded by a glial scar is observed [2].

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