Alpha-2 adrenergic and Cyclo-Oxygenase Mechanisms in Lipopolysaccharide-induced neuropathic pain in Rats

Abstract

The mechanism by which tissue injuries produces a state of neuropathic pain represent one of the most intensely investigated areas in the biomedical science over several cascades. Hence, a substantial body of evidence gathered from a variety of disease points to a critical interaction between the sympathetic nervous and the inflammatory cascade. The present study explored the probable action of the synergistic effects of adrenergic neurotransmission and cyclo-oxygenase inhibition in lipopolysaccharide-induced neuropathic pain in male Wistar rats. Wistar rats (225–250) g was used for this study. Neuropathic pain was induced with the systematic administration of 250μg/mg lipopolysaccharide (LPS). The effects of sulindac sulfide, yohimbine, and naphazoline on the movement were accessed using the Morris water maze model. Histological analysis using Nissl staining techniques and biochemical assay were evaluated. Peripheral administration of LPS was showed to reduce cognitive and locomotor process. The result of the LPS only showed a significant decreased in protein, GSH, SOD concentration and increased in MDA level when compared to control. However, drugs co-administered were shown to significantly ameliorate the decrease in antioxidant defense. Histology shows that the damage caused by LPS to the brain neurons was markedly reduced by the administration of the synergistic action of the adrenergic receptor pathway and COX inhibition pathway. These findings suggest that the synergistic action of both pathways might be beneficial in the management of neuropathic pain