Abstract
Methylprednisolone (MP), a synthetic glucocorticoid, has been widely used as a standard therapeutic agent for the treatment of spinal cord injury (SCI). The combination of MP and other pharmacological agents aimed at enhancing functional recovery is desirable as the beneficial effects of MP are controversial, due to a variety of side-effects. Aminoguanidine (AG), a small water-soluble compound, is potentially useful in the treatment of acute SCI. The aim of the present study was to determine the effects of MP and AG, administered in combination, following SCI in adult rats. In rats with SCI, the combination therapy group treated with AG (75 mg/kg) and MP (0.75 mg/kg) exhibited significantly reduced levels of cytokine expression and cell apoptosis compared with those in the control group. In addition, the data demonstrated that the combination therapy significantly enhanced the recovery of limb function. These data clearly suggest that treatment with a combination of MP and AG represents a promising strategy of clinically applicable pharmacological therapy for the rapid initiation of neuroprotection following SCI.
Highlights
The pathophysiology of traumatic spinal cord injury (SCI) is thought to divide into two stages [1]
The present study provides convincing evidence that the combination of MP with AG significantly reduced the levels of spinal cord edema and improved the damaged motor function caused by SCI in rats, whereas a single treatment did not significantly improve them
The enhanced viability and regenerative capacity of neurons and functional recovery supported by MP and AG combination treatment has practical and conceptual implications due to the proinflammatory effect on neurons in vivo following experimental SCI [19,27,28]
Summary
The pathophysiology of traumatic spinal cord injury (SCI) is thought to divide into two stages [1]. The spinal cord is a glucocorticoid‐responsive tissue and it contains substantial amounts of receptors for adrenocortical steroids [5,6]. Methylprednisolone (MP) is a synthetic glucocorticoid and the only therapeutic agent approved by the Food and Drug Administration for reducing the extent of the post‐traumatic inflammatory reaction following acute SCI [9,10]. The application of MP after SCI is associated with a wide array of anti‐inflammatory effects, including anti‐lipid peroxidation [11,12] and attenuation of the formation of deleterious prostanoids (prostaglandin F2α and thromboxane A2) [13], the long‐term administration of this therapeutic steroid results in a variety of side‐effects, such as downregulation of the expression of several inflammatory genes and an inhibitory effect on the proliferation of endogenous neural progenitor cells following SCI [14]
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