The effect of etanercept on spinal epidural fibrosis in a postlaminectomy rat model.

AIM: The formation of epidural fibrosis adjacent to the dura mater after posterior spinal surgery is a normal reaction of the body to surgery. Extensive epidural fibrosis is one of the important causes of postlaminectomy syndrome. Etanercept inhibits tumor necrosis factor-alpha and decreases fibroblast migration. Thus, etanercept prevents the formation of fibrosis. The aim of this study was to investigate the effects of topical application of etanercept on epidural fibrosis after laminectomy in a rat model. MATERIAL AND METHODS: Twenty-four Wistar rats were equally and randomly divided into three groups (control, spongostan and etanercept). Laminectomy was performed between L3 and L5 in all the rats. Spongostan soaked with saline (0.1 mg/kg) and etanercept (300 µg/kg) was directly exposed to and left on the dura mater. Four weeks later, the vertebral columns of the rats were removed en bloc between T10 and L5, and epidural fibrosis and arachnoidal involvement were evaluated and graded histopathologically. RESULTS: Our data revealed that epidural fibrosis was reduced significantly in the rats treated with etanercept, compared to the control groups (p < 0.05). CONCLUSION: Our study demonstrated that topical application of etanercept can be effective in reducing epidural fibrosis in rats after laminectomy.

Use of decorin to prevent epidural fibrosis in a post-laminectomy rat model.

The formation of epidural fibrosis adjacent to the dura mater is a complex multi-step process that is associated with a marked reduction in tissue cellularity and the excessive deposition of extracellular matrix components. Extensive epidural fibrosis is a major cause of post-laminectomy syndrome. Decorin strongly inhibits fibrosis formation in various tissues via blockade of transforming growth factor-ß1. The aim of this study was to investigate the effects of a topical application of decorin on the formation of epidural fibrosis in a rat laminectomy model. Twenty-four female Wistar albino rats (250-350 g) were equally and randomly divided into three groups (control, spongostan and decorin). Laminectomy was performed between the L3 and L5 levels in all rats. The dura mater was directly exposed to spongostan soaked with saline (2 cc/kg) or decorin (100 µg/kg). Four weeks later, the laminectomized spine of the rats was completely removed between the L3 and L5 levels. The extent of the epidural fibrosis and arachnoidal involvement was histopathologically evaluated and graded. Our data revealed that epidural fibrosis was significantly reduced in the group treated with decorin compared to the spongostan and control groups (P<0.05). Our study demonstrates that the topical application of decorin can be effective in reducing the formation of epidural fibrosis in a simple laminectomy rat model.

Effects of α-MSH on ischemia/reperfusion injury in the rat sciatic nerve.

BACKGROUND: Ischemia/reperfusion (I/R) causes the production of toxic free radicals and leads to pathological changes in nerve tissue. We investigated the effect of alpha-melanocyte stimulating hormone (α-MSH) in a rat model for sciatic nerve I/R and discuss the possible cytoprotective and antioxidant mechanism of α-MSH against ischemic fiber degeneration. METHODS: Experiments were performed using 42 adult male Wistar rats. Rats were divided into six experimental groups: control group, ischemia group, I/R groups, and α-MSH treated groups. Ischemia was produced by clamping of the femoral vessels. Immediately after ischemia that lasted 3 h, 75 µg/kg of α-MSH was administered subcutaneously before reperfusion and the tissue malondialdehyde (MDA) level was evaluated as an indicator of lipid peroxidation in groups with different reperfusion periods. RESULTS: The reperfusion injury did not begin in the first hour of reperfusion after 3 h of ischemia, and MDA levels increased on the first day of reperfusion. During the first day, blood MDA levels were decreased in the α-MSH group compared to the control group. The tissue from animals pre-treated with α-MSH showed fewer morphological alterations. Myelin breakdown was significantly diminished after treatment with α-MSH, and the ultrastructural features of axons showed remarkable improvement. Two-way analysis of variance was used for comparing three or more groups. When a significant difference existed, the post-hoc multiple-comparison test was applied to demonstrate the differences. CONCLUSIONS: The results confirm that pre-treatment with α-MSH after ischemia protected the peripheral nerves against I/R injury.

Effect of curcumin on lipid peroxidation, early ultrastructural findings and neurological recovery after experimental spinal cord contusion injury in rats.

AIM: After acute spinal cord injury (SCI), a large number of axons are lost by a cascade of pathophysiological events known as a secondary injury. The main aim of the current study was to investigate the potential neuroprotective effects of curcumin on lipid peroxidation (LPO), neurological function, and ultrastructural findings after SCI. MATERIAL AND METHODS: Forty adult Wistar albino rats were randomized into five groups: control, SCI alone (50 g/cm weight drop), methylprednisolone sodium succinate (MPSS) (30 mg/kg), curcumin + dimethyl sulfoxide (DMSO) (300 mg/kg), and DMSO alone (0.1 mg/kg). RESULTS: Administration of curcumin significantly decreased LPO in first 24 hours. However, there were no differences in the neurological scores of injured rats between the medication groups and the control group. Curcumin was more effective than DMSO and MPSS in reducing LPO, whereas DMSO was more effective than curcumin and MPSS in minimizing ultrastuctural changes. The results of this study indicate that curcumin exerts a beneficial effect by decreasing LPO and may reduce tissue damage. CONCLUSION: Since ultrastructural and neurological findings does not support biochemical finding, our findings do not exclude the possibility that curcumin has a protective effect on the spinal cord ultrastructure and neurological recovery after SCI. A combination of curcumin with other vehicle may also have a considerable synergy in protecting spinal cord.

Methothrexate attenuates early neutrophil infiltration and the associated lipid peroxidation in the injured spinal cord but does not induce neurotoxicity in the uninjured spinal cord in rats.

BACKGROUND: The goal of most acute therapies for spinal cord injury (SCI) in humans include attenuation of the early inflammatory response and may limit the extent of tissue injury and the consequent disability. OBJECTIVE: The purpose of this study was to investigate the early effects of methothrexate (MTX) treatment on myeloperoxidase (MPO) activity, malondialdehyde (MDA) level, and ultrastructural findings in the injured and uninjured spinal cords of rats. The effects of MTX treatment were also compared with methylprednisolone sodium succinate (MPSS) treatment. METHODS: Wistar rats were divided into seven groups: control; trauma alone (50 g/cm weight drop trauma); SCI + MPSS (30 mg/kg); SCI + low-dose (0.5 mg/kg) MTX (LDMTX); SCI + higher-dose (1 mg/kg) MTX (HDMTX); non-trauma + LDMTX; non-trauma + HDMTX. RESULTS: Administration of MTX and MPSS treatments significantly decreased MPO activity (p < 0.05) and MDA level (p < 0.05) in the first 24 h. The MTX treatments, particularly HDMTX, were more effective than MPSS in reducing MPO activity, and MTX treatments were also more effective than MPSS in reducing MDA level (p < 0.05). The MTX treatment was more protective on large- and medium-diameter myelinated axons in minimizing ultrastructural changes in the spinal-cord-injured rats, but did not induce neurotoxicity in normal spinal cord. CONCLUSION: The results of this study indicate that MTX treatment has a beneficial effect by reducing early neutrophil infiltration and the associated lipid peroxidation, and has significantly protective effects on the injured spinal cord tissue in the first 24 h after SCI. Given the anti-inflammatory properties of MTX, a single dose of MTX a week is used for non-neoplastic disease in humans, and MTX may have a beneficial role in the immediate management of acute SCI.

Effect of granulocyte-colony stimulating factor on spinal cord tissue after experimental contusion injury.

The purpose of this study was to investigate the early effects of granulocyte-colony stimulating factor (G-CSF) on myeloperoxidase (MPO) activity, lipid peroxidation (LPO) and ultrastructural findings in rats after spinal cord injury (SCI). We also compared the effects of G-CSF and methylprednisolone sodium succinate (MPSS). Wistar rats were divided into four groups: control, SCI alone (50 g/cm weight drop trauma), SCI+MPSS (30 mg/kg), and SCI+G-CSF (50 µg/kg). Administration of G-CSF and MPSS significantly decreased LPO (p < 0.05) and MPO activity (p < 0.05) in the first 24 hours. MPSS was more effective than G-CSF in reducing LPO (p < 0.05) and in minimizing ultrastructure changes. The results of this study indicate that G-CSF exerts a beneficial effect by decreasing MPO activity and LPO and may reduce tissue damage in the first 24 hours after SCI. Our findings do not exclude the possibility that G-CSF has a protective effect on spinal cord ultrastructure after the first 24 hours following SCI.

Chronic subdural hematoma in capoeira sport.

Chronic subdural hematomas in young people is extremely rare and has some provoking factors such as V-P shunts, arachnoid cyst, anticoagulant drug usage, vigorous sports and coagulopathies. A static or dynamic mechanical load is almost always delivered to skull associated with either mild or severe head trauma. A 25-year old-man who was previously healthy has complained of intermittent headache for six months. He had been interested in capoiera (Brazilian exciting sport) for two years and has had no any evidence of head injury. After admission, he was operated immediately because of chronic subdural hematoma. We report a patient who is the first chronic subdural hematoma in the literature due to playing capoeira.