Decreased GFAP Expression and Improved Functional Recovery in Contused Spinal Cord of Rats Following Valproic Acid Therapy

Abstract

Many studies have illustrated that much of the post-traumatic degeneration of the spinal cord cells is caused by the secondary mechanism. The aim of this study is to evaluate the effect of the anti-inflammatory property of valproic acid (VPA) on injured spinal cords (SC). The rats with the contused SC received intraperitoneal single injection of VPA (150, 200, 300, 400 or 500 mg/kg) at 2, 6, 12 and 24 h post-injury. Basso-Beattie-Bresnahan (BBB) test and H-reflex evaluated the functional outcome for 12 weeks. The SC were investigated 3 months post-injury using morphometry and glial fibrillary acid protein (GFAP) expression. Reduction in cavitation, H/M ratio, BBB scores and GFAP expression in the treatment groups were significantly more than that of the untreated one (P < 0.05). The optimal improvement in the condition of the contused rats was in the ones treated at the acute phase of injury with 300 mg/kg of VPA at 12 h post-injury, they had the highest increase in BBB score and decrease in astrogliosis and axonal loss. We conclude that treating the contused rats with 300 mg/kg of VPA at 12 h post-injury improves the functional outcome and reduces the traumatized SC gliosis.

5‐Nonyloxytryptamine oxalate–embedded collagen–laminin scaffolds augment functional recovery after spinal cord injury in mice

“…Darvishi et al . reported a decrease in GFAP expression after the treatment with valproic acid in SCI rats resulted in improved functional recovery …”

Therapeutic Effect of Curcumin and Methylprednisolone in the Rat Spinal Cord Injury

“…In secondary injury, acute inflammation can develop into a chronic process as feedback mechanisms fail to inhibit the amplification of the inflammatory response (Evaniew et al, ). Owing to inflammation having a role in the instigation of SCI, truncating the inflammatory process could possibly contribute to reduction of the secondary mechanism of SCI (Darvishi et al, ). Astrocytes are major cell types in the spinal cord and provide a variety of critical supportive functions that establish and maintain neuronal homeostasis and upregulate the expression of GFAP (Tian et al, ; Li et al, ).…”

“…Inflammation is one of the important factors in the secondary mechanism of SCI. Inflammatory responses play a pivotal role in the pathogenesis, which in turn leads to neuronal death and formation of glial scar, along with the eventual loss of neuronal functions (Darvishi et al, ). The key to functional recovery of SCI is to minimize cell death of glial and neuronal cells, scarring and cavitation whiles blocking inhibitory molecules in the lesion area as well as stimulating functional axonal regeneration (Zeng et al, ).…”

“…The key to functional recovery of SCI is to minimize cell death of glial and neuronal cells, scarring and cavitation whiles blocking inhibitory molecules in the lesion area as well as stimulating functional axonal regeneration (Zeng et al, ). For that reason, reducing the inflammatory process could contribute to the diminution of the secondary mechanism (Darvishi et al, ). The glial scar tissue is often seen as a biochemical and physical barrier against the growth of axons (Luan et al, ).…”

Resveratrol treatment of spinal cord injury in rat model

“…Inflammatory responses play an important role in SCI pathogenesis that causes neural cell apoptosis or necrosis and glial hyperplasia. These can lead to formation of glial scar, axonal regeneration failure as well as eventual loss of motor and sensory functions (Darvishi, Tiraihi, Mesbah‐Namin, Delshad, & Taheri, ; Xu et al, ). The key to functional recovery following SCI lies in anti‐inflammation, neuroprotection, and neuroregeneration combinational approaches in reducing scarring and cavitation, blocking inhibitory molecules, and stimulating functional axonal regeneration at lesion area (Requejo‐Aguilar et al, ; Zeng et al, ).…”