OBJECTIVETo investigate the protective effect of antler polypeptide on the rats with spinal cord injury (SCI).

METHODSThe model rats were treated with different doses of antler polypeptide, and its effect on motor function, ethology and pathological changes of spinal cord of the rats observed.

RESULTSSeven days after treatment with different doses of antler polypeptide, rat's motor activity was recovered in some extent. Significant difference (P < 0.001)was found between the antler polypeptide treatment group and operation group. The effect could be enhanced by increase of the doses. We observerd the effect on the pathological change of spinal cord in rat, and found the tissue edema and inflammatory infiltration were relieved after treatment with different doses of antler polypeptide, especially in the dose of 15 mg antler polypeptide.

CONCLUSIONAntler polypeptide can promote the motor function recovery in SCI rats, and its action is dose-dependent.

Animals ; Antlers ; chemistry ; Male ; Peptides ; therapeutic use ; Rats ; Rats, Wistar ; Spinal Cord ; pathology ; Spinal Cord Injuries ; drug therapy ; pathology

Recent clinical trials have reported that methylprednisolone sodium succinate administered within 8 hours improves neurological recovery in human spinal cord injury (SCI). Methylprednisolone, however, was ineffective and possibly even deleterious when given more than 8 hours after injury. This finding suggests that a therapeutic time window exists in spinal cord injury. In order to determine the doses, durations and timing of methylprednisolone treatment for optimal neuroprotection, a single or two bolus dose of methylprednisolone (30 mg/kg) was administered at 10, 30, 120, 150 and 240 min. after three graded spinal cord injury. The primary outcome measure was 24-hour spinal cord lesion volumes estimated from spinal cord Na+ and K+ shifts. A single 30 mg/kg dose of methylprednisolone at 10 min. after injury significantly reduced 24-hour lesion volumes in injured rat spinal cords. However, any other methylprednisolone treatment starting 30 min. or more after injury had no effect on 24-hour lesion volumes compared to the vehicle control group. Moreover, delayed treatment increased lesion volumes in some cases. These results suggest that the NYU SCI model has a very short therapeutic window.
Animal ; Drug Administration Schedule ; Male ; Methylprednisolone Hemisuccinate/therapeutic use ; Methylprednisolone Hemisuccinate/administration & dosage* ; Neuroprotective Agents/therapeutic use ; Neuroprotective Agents/administration & dosage* ; Rats ; Rats, Long-Evans ; Spinal Cord/pathology ; Spinal Cord Injuries/pathology ; Spinal Cord Injuries/drug therapy*

BACKGROUNDThe iron catalyzed lipid peroxidation plays an important role in the autodestruction of the injured spinal cord. This study was to detect the antioxidation of melatonin against spinal cord injury (SCI) in rats.

METHODSSity Sprague-Dawley rats were randomly divided into four groups: group A (n = 15) for laminectomyanly, group B (n = 15) for laminectomy with SCI, group C (n = 15) for SCI and intraperitoneal injection of a bolus of 100 mg/kg melatonin, and group D (n = 15) for SCI and intraperitoneal injection of saline containing 5% ethanol. The SCI of animal model was made using modified Allen's method on T12. Six rats of each group were sacrificed 4 hours after injury, and the levels of free iron and malondialdehyde (MDA) of the involved spinal cord segments were measured by the bleomycin assay and thiobarbituric acid (TBA) separately. Functional recovery of the spinal cord was assessed by Modified Tarlov's scale and the inclined plane method at 1, 3, 7, 14, 21 days after SCI. The histologic changes of the damaged spinal cord were also examined at 7 days after SCI.

RESULTSAfter SCI, the levels of free iron and MDA were increased significantly and the modified Tarlov's score and inclined plane angle decreased significantly in groups B and D. In group C, the Tarlov's score and inclined plane angle were increased significantly at 7, 14 and 21 days, with histological improvement.

CONCLUSIONMelatonin can reduce the level of lipid peroxidation and prevent damage to the spinal cord of rat.

Animals ; Antioxidants ; therapeutic use ; Iron ; analysis ; Lipid Peroxidation ; drug effects ; Male ; Malondialdehyde ; analysis ; Melatonin ; therapeutic use ; Rats ; Rats, Sprague-Dawley ; Spinal Cord Injuries ; drug therapy ; metabolism ; pathology

OBJECTIVETo observe the effect of quercetin on experimental spinal cord injury (SCI) in rats.

METHODSSixty Sprague-Dawley rats were randomly divided into four groups: Group A only for laminectomy, Group B for laminectomy with SCI, Group C for SCI and intraperitoneal injection with a bolus of 200 mg/kg quercetin and Group D for SCI and intraperitoneal injection of saline. SCI model was made by using modified Allen's method on T(12). Six rats of each group were killed at 4 h after injury and the levels of free iron and malondialdehyde (MDA) of the involved spinal cord segments were measured by bleomycin and thiobarbituric acid (TBA) assays separately. The recovery of hind limb function was assessed by Modified Tarlov's scale and inclined plane method at 7 d, 14 d and 21 d after SCI. The histological changes of the damaged spinal cord were also examined at 7 d after SCI.

RESULTSAfter SCI, the levels of free iron and MDA were significantly increased in Groups B and D, while not in Group C. The Modified Tarlov's score and the inclined plane angles were significantly decreased in Groups B, C and D. The histological findings were not improved.

CONCLUSIONSAfter SCI, quercetin can reduce the level of lipid peroxidation, but not improve recovery of function.

Animals ; Antioxidants ; therapeutic use ; Iron ; analysis ; Male ; Malondialdehyde ; analysis ; Quercetin ; therapeutic use ; Rats ; Rats, Sprague-Dawley ; Spinal Cord Injuries ; drug therapy ; metabolism ; pathology

Evidence suggested that glycogen synthase kinase-3β (GSK-3β) is involved in Nogo-66 inhibiting axonal regeneration in vitro, but its effect in vivo was poorly understood. We showed that stereotactic injection of shRNA GSK-3β-adeno associated virus (GSK-3β-AAV) diminished syringomyelia and promoted axonal regeneration after spinal cord injury (SCI), using stereotactic injection of shRNA GSK-3β-AAV (tested with Western blotting and RT-PCR) into the sensorimotor cortex of rats with SCI and by the detection of biotin dextran amine (BDA)-labeled axonal regeneration. We also determined the right position to inject into the sensorimotor cortex. Our findings consolidate the hypothesis that downregulation of GSK-3β promotes axonal regeneration after SCI.
Animals ; Axons ; drug effects ; metabolism ; Dependovirus ; genetics ; Glycogen Synthase Kinase 3 beta ; genetics ; metabolism ; Humans ; Nerve Regeneration ; genetics ; RNA, Small Interfering ; administration & dosage ; genetics ; Rats ; Sensorimotor Cortex ; drug effects ; pathology ; Spinal Cord Injuries ; genetics ; pathology ; therapy ; Syringomyelia ; genetics ; pathology ; therapy

OBJECTIVETo investigate the clinical characteristics and results of cervical spinal cord injury (SCI) in the patients with ossification of the posterior longitudinal ligament (OPLL).

METHODSNineteen patients with cervical SCI associated with OPLL were retrospectively analyzed. Data collection included: pre- and postoperative neurological function, OPLL-type, MRI signal changes and surgical approaches.

RESULTSSpinal cord associated with OPLL was injured severely by mild trauma. Methylprednisolone sodium succinate was used within 8 h after trauma in 12 cases. Two of them died of complications. The neurological functions were markedly improved in the other 10 cases. Seventeen cases had surgical treatment. The neurological functions (Frankel grade) were improved significantly in the operated patients except for one, who died 27 d after operation.

CONCLUSIONSThe patients with OPLL are prone to have severe SCI, which directly associates with the preexisting OPLL-type and hyper-intensity signal change in the spinal cord on MRI. Both of using methylprednisolone sodium succinate administration within 8 h after trauma and surgical decompression may improve the neurological outcomes.

Aged ; Cervical Vertebrae ; Decompression, Surgical ; Female ; Follow-Up Studies ; Glucocorticoids ; therapeutic use ; Humans ; Longitudinal Ligaments ; pathology ; Male ; Middle Aged ; Ossification of Posterior Longitudinal Ligament ; complications ; Retrospective Studies ; Spinal Cord ; drug effects ; physiopathology ; surgery ; Spinal Cord Injuries ; diagnosis ; etiology ; therapy ; Spinal Stenosis ; diagnosis ; etiology ; therapy ; Treatment Outcome

Methylprednisolone (MP), a glucocorticoid steroid, has an anti-inflammatory action and seems to inhibit the formation of oxygen free radicals produced during lipid peroxidation in a spinal cord injury (SCI). However, the effects of MP on the functional recovery after a SCI is controversial. The present study was conducted to determine the effects of MP on the recovery of neural conduction following a SCI. A SCI was produced using the NYU spinal cord impactor. A behavioral test was conducted to measure neurological disorders, and motor evoked potentials (MEPs) were recorded. According to the behavioral test, using BBB locomotor scaling, MP-treated animals showed improved functional recoveries when compared to salinetreated animals. MEP latencies in the MP-treated group were shortened when compared to those in the control group. Peak amplitudes of MEPs were larger in the MP-treated group than those in the control group. The thresholds of MEPs tended to be lower in the MP-treated group than those in the control group. These results suggest that MP may improve functional recovery after a SCI.
Animals ; Disease Models, Animal ; Electrophysiology ; Evoked Potentials, Motor/*drug effects ; Free Radicals ; Glucocorticoids/metabolism ; Male ; Methylprednisolone/*pharmacology ; Neurons/*drug effects ; Oxygen/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Glucocorticoid/metabolism ; Research Support, Non-U.S. Gov't ; Sodium Chloride/pharmacology ; Spinal Cord/pathology ; Spinal Cord Injuries/*drug therapy ; Time Factors

OBJECTIVETo determine the effects of recombinant soluble complement receptor type I (sCR1) on the immune inflammatory reaction in acute spinal cord injury tissue of rats and its protective effects.

METHODSSD rat models of acute spinal cord injury were prepared by modified Allen's method. The motor function of the rat lower extremities in sCR1 group and normal saline (NS) group was evaluated by the tiltboard experiment at 12 h, 1 d, 3 d, 7 d, and 14 d. The neutrophil infiltration and C3c positive expression were observed. The myeloperoxidase activity was assessed in the injury tissue at 12 h, 1 d, 3 d, 7 d, and 14 d after injury in the two groups.

RESULTSThe motor function of rat in sCR1 group at 3 d, 7 d, and 14 d was obviously better than that in NS group (P<0.01, P<0.01, P<0.01). C3c positive expression in sCR1 group at each time point after injury was obviously less than that in NS group (P<0.01). The myeloperoxidase activity in sCR1 group at each time point after injury was obviously less than that in NS group (P<0.01).

CONCLUSIONSRecombinant soluble complement receptor type I (sCR1) can lessen the immune inflammatory reaction in acute spinal cord injury tissue and relieve secondary spinal cord injury by inhibiting the activation of the complement system.

Animals ; Disease Models, Animal ; Immunohistochemistry ; Inflammation ; Peroxidase ; biosynthesis ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptors, Complement ; therapeutic use ; Recombinant Proteins ; therapeutic use ; Spinal Cord Injuries ; drug therapy ; enzymology ; pathology

As one of trials on neuroprotection after spinal cord injury, we used pregabalin. After spinal cord injury (SCI) in rats using contusion model, we observed the effect of pregabalin compared to that of the control and the methylprednisolone treated rats. We observed locomotor improvement of paralyzed hindlimb and body weight changes for clinical evaluation and caspase-3, bcl-2, and p38 MAPK expressions using western blotting. On histopathological analysis, we also evaluated reactive proliferation of glial cells. We were able to observe pregabalin's effectiveness as a neuroprotector after SCI in terms of the clinical indicators and the laboratory findings. The caspase-3 and phosphorylated p38 MAPK expressions of the pregabalin group were lower than those of the control group (statistically significant with caspase-3). Bcl-2 showed no significant difference between the control group and the treated groups. On the histopathological analysis, pregabalin treatment demonstrated less proliferation of the microglia and astrocytes. With this animal study, we were able to demonstrate reproducible results of pregabalin's neuroprotection effect. Diminished production of caspase-3 and phosphorylated p38 MAPK and as well as decreased proliferation of astrocytes were seen with the administration of pregabalin. This influence on spinal cord injury might be a possible approach for achieving neuroprotection following central nervous system trauma including spinal cord injury.
Animals ; Apoptosis/drug effects ; Astrocytes/drug effects/pathology ; Blotting, Western ; Body Weight/drug effects ; Caspase 3/genetics ; Cell Proliferation ; Fluorescent Antibody Technique ; Gene Expression ; Hindlimb/drug effects/pathology/physiopathology ; Inflammation ; Male ; Methylprednisolone/therapeutic use ; Microglia/drug effects/pathology ; Motor Activity/drug effects ; Neuroglia/*drug effects/pathology ; Neuroprotective Agents/*therapeutic use ; Paralysis/drug therapy ; Proto-Oncogene Proteins c-bcl-2/genetics ; Rats ; Rats, Sprague-Dawley ; Spinal Cord Injuries/*drug therapy/pathology ; gamma-Aminobutyric Acid/*analogs & derivatives/therapeutic use ; p38 Mitogen-Activated Protein Kinases/genetics

Transcatheter arterial chemoembolization (TACE) has been used widely to treat patients with unresectable hepatocellular carcinoma. However, this method can induce various adverse events caused by necrosis of the tumor itself or damage to nontumor tissues. In particular, neurologic side effects such as cerebral infarction and paraplegia, although rare, may cause severe sequelae and permanent disability. Detailed information regarding the treatment process and prognosis associated with this procedure is not yet available. We experienced a case of paraplegia that occurred after conducting TACE through the intercostal artery to treat hepatocellular carcinoma that had metastasized to the rib. In this case, TACE was attempted to relieve severe bone pain, which had persisted even after palliative radiotherapy. A sudden impairment of sensory and motor functions after TACE developed in the trunk below the level of the sternum and in both lower extremities. The patient subsequently received steroid pulse therapy along with supportive care and continuous rehabilitation. At the time of discharge the patient had recovered sufficiently to enable him to walk by himself, although some paresthesia and spasticity remained.
Antiviral Agents/therapeutic use ; Bone Neoplasms/radiography/secondary ; Carcinoma, Hepatocellular/diagnosis/pathology/*therapy ; Catheter Ablation ; Chemoembolization, Therapeutic/*adverse effects ; Hepatitis B/complications/drug therapy ; Humans ; Liver Cirrhosis/etiology ; Liver Neoplasms/diagnosis/pathology/*therapy ; Male ; Middle Aged ; Positron-Emission Tomography ; Soft Tissue Neoplasms/secondary ; Spinal Cord Injuries/*etiology ; Tomography, X-Ray Computed