Effects of astaxanthin on sensory-motor function in a compression model of spinal cord injury: Involvement of ERK and AKT signaling pathway.

BACKGROUND: Spinal cord injury (SCI) causes continuous neurological deficits and major sensory-motor impairments. There is no effective treatment to enhance sensory-motor function following SCI. Thus, it is crucial to develop novel therapeutics for this particular patient population. Astaxanthin (AST) is a strong anti-oxidant, anti-inflammatory, and anti-apoptotic agent. In the present study, it was tested in a severe compression SCI model with emphasis on sensory-motor outcomes, signaling pathway, along with other complications.

METHODS: A severe SCI was induced by compression of the rat thoracic spinal cord with an aneurysm clip and treatment with AST or the vehicle were done, 30 min after injury. Behavioral tests including open field, von Frey, hot plate, and BBB were performed weekly to 28 days post-injury. Rats were assigned to measure blood glucose, weight, and auricle temperature. Western blot and histological analysis also were done at the same time points.

RESULTS: AST decreased mechanical and thermal pain and also improved motor function performance, reduced blood glucose and auricle temperature increases, and attenuated weight loss in SCI rats. Western blot analysis showed decreased activation of ERK1/2 and increased activation of AKT following AST treatment. The histology results revealed that AST considerably preserved myelinated white matter and the number of motor neurons following SCI.

CONCLUSION: Taken together, the beneficial effects of AST to improve sensory-motor outcomes, attenuate pathological tissue damage, and modulate ERK and Akt signaling pathways following SCI, suggest it as a strong therapeutic agent toward clinical applications. This article is protected by copyright. All rights reserved.