Abstract

AimsImmunization with neural‐derived peptides (INDP) has demonstrated to be a promising therapy to achieve a regenerative effect in the chronic phase of the spinal cord injury (SCI). Nevertheless, INDP‐induced neurogenic effects in the chronic stage of SCI have not been explored.Methods and ResultsIn this study, we analyzed the effect of INDP on both motor and sensitive function recovery; afterward, we assessed neurogenesis and determined the production of cytokines (IL‐4, IL‐10, and TNF alpha) and neurotrophic factors (BDNF and GAP‐43). During the chronic stage of SCI, rats subjected to INDP showed a significant increase in both motor and sensitive recovery when compared to the control group. Moreover, we found a significant increase in neurogenesis, mainly at the central canal and at both the dorsal and ventral horns of INDP‐treated animals. Finally, INDP induced significant production of antiinflammatory and regeneration‐associated proteins in the chronic stages of SCI.ConclusionsThese findings suggest that INDP has a neurogenic effect that could improve motor and sensitive recovery in the chronic stage of SCI. Moreover, our results also envision the use of INDP as a possible therapeutic strategy for other trauma‐related disorders like traumatic brain injury.

Highlights

  • Immunization with neural derived peptides (INDP) has demonstrated to be a promising therapy to achieve a regenerative effect in the chronic phase of the spinal cord injury (SCI)

  • These findings suggest that INDP has a neurogenic effect that could improve motor and sensitive recovery in the chronic stage of SCI

  • In order to test the effect of INDP on neurological recovery, we first evaluated the motor performance of SCI rats compared to the phosphate buffered saline (PBS) group

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Summary

Introduction

Immunization with neural derived peptides (INDP) has demonstrated to be a promising therapy to achieve a regenerative effect in the chronic phase of the spinal cord injury (SCI). Spinal cord injury (SCI) is a severe medical condition generally caused by a traumatic mechanism, such as contusion, compression or transection. The secondary phase occurs within 2 hours and 6 months after injury [5, 6] During this phase, the injury increases by the action of pro-inflammatory factors, excitotoxicity, vascular alterations, oxidative stress, and ischemia. The injury increases by the action of pro-inflammatory factors, excitotoxicity, vascular alterations, oxidative stress, and ischemia These destructive mechanisms show a gradual decrease until the chronic stage of injury, where they are almost at its minimum expression; there is still a progressive decline in the neurological function [7]. Several strategies have been tested in order to promote neural restoration [8]

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