Abstract

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 antioxidant, 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, signalling pathway, along with other complications. A severe SCI was induced by compression of the rat thoracic spinal cord with an aneurysm clip and treatment with AST or the vehicle was carried out, 30min after injury. Behavioural tests including open field, von Frey, hot plate and BBB were performed weekly to 28days post-injury. Rats were assigned to measure blood glucose, weight and auricle temperature. Western blot and histological analysis also were performed at the same time points. 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. Taken together, the beneficial effects of AST to improve sensory-motor outcomes, attenuate pathological tissue damage and modulate ERK and AKT signalling pathways following SCI, suggest it as a strong therapeutic agent towards clinical applications. Spinal cord injury (SCI) impairs sensory-motor function and causes complications, which astaxanthin (AST) has the potential to be used as a treatment for. The present study investigates the effects of AST in a compression model of SCI with emphasis on sensory-motor outcomes alongside other complications, histopathological damage and also related signalling pathways.

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