Abstract
Well known for its anti-oxidative and anti-inflammation properties, curcumin is a polyphenol found in the rhizome of Curcuma longa. In this study, we evaluated the effects of curcumin on behavioral recovery, glial scar formation, tissue preservation, axonal sprouting, and inflammation after spinal cord injury (SCI) in male Wistar rats. The rats were randomized into two groups following a balloon compression injury at the level of T9–T10 of the spinal cord, namely vehicle- or curcumin-treated. Curcumin was applied locally on the surface of the injured spinal cord immediately following injury and then given intraperitoneally daily; the control rats were treated with vehicle in the same manner. Curcumin treatment improved behavioral recovery within the first week following SCI as evidenced by improved Basso, Beattie, and Bresnahan (BBB) test and plantar scores, representing locomotor and sensory performance, respectively. Furthermore, curcumin treatment decreased glial scar formation by decreasing the levels of MIP1α, IL-2, and RANTES production and by decreasing NF-κB activity. These results, therefore, demonstrate that curcumin has a profound anti-inflammatory therapeutic potential in the treatment of spinal cord injury, especially when given immediately after the injury.
Highlights
Spinal cord injury (SCI) is a devastating medical condition that can temporarily or permanently impair sensory and motor functions
SCI consists of a two-step process involving the initial physical injury leading to a progressive injury process that comprises glial scar formation, inflammation, lipid peroxidation, and glutamate excitotoxicity
Many studies in recent years have investigated a variety of pharmacological interventions targeting these secondary processes, such as methylprednisolone, melatonin, erythropoietin, and naloxone, all of which resulted in only a slight improvement of impaired function after SCI
Summary
Spinal cord injury (SCI) is a devastating medical condition that can temporarily or permanently impair sensory and motor functions. SCI consists of a two-step process involving the initial physical injury leading to a progressive injury process (secondary injury) that comprises glial scar formation, inflammation, lipid peroxidation, and glutamate excitotoxicity. Secondary processes that result in glial scar formation and hinder recovery evolve within hours to days. Many studies in recent years have investigated a variety of pharmacological interventions targeting these secondary processes, such as methylprednisolone, melatonin, erythropoietin, and naloxone, all of which resulted in only a slight improvement of impaired function after SCI. Behavioral performance, glial scar formation, tissue preservation, axonal sprouting, the activity of NF-κB transcription factor, and the levels of proinflammatory cytokines were evaluated after experimental SCI to elucidate the mechanisms underlying the effect of curcumin on spinal cord lesion development
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