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

Child ; Germinoma ; chemistry ; pathology ; surgery ; Humans ; Immunohistochemistry ; Male ; Spinal Cord Neoplasms ; chemistry ; pathology ; surgery

A case of spinal meningeal melanocytoma is reported along with clinicopathologic, immunohistochemical and ultrastructural studies. This patient presented clinically with paraparesis, tingling sensation and numbness of both lower extremities of 4 months duration. No mucocutaneous pigmented nevi were found. On operation, scattered coal-black pigmented lesions were found in the meninges between T3 and T4-5 interspace level. Nearly total removal was carried out. The tumor was composed of spindle and epithelioid cells with heavy brown-black pigmentation. There was no pleomorphism, mitosis, hemorrhage, necrosis or invasion to the underlying cord tissue. In Korea, this case appears to be the first example of this disease. Neurologic deficit improved after surgical excision.
Adult ; Female ; Humans ; Immunoenzyme Techniques ; Meningeal Neoplasms/chemistry/*pathology/ultrastructure ; Microscopy, Electron ; Spinal Cord

Melatonin (N-acetyl-5-methoxytryptamine), a pineal neurohormone, is a hydroxyl radical scavenger and antioxidant, and plays an important role in the immune system. We studied the effect of exogenous melatonin on the pathogenesis of experimental autoimmune encephalomyelitis (EAE). EAE was induced in Lewis rats by immunization with rat spinal cord homogenates. Subsequent oral administration of melatonin at 5 mg/kg significantly reduced the clinical severity of EAE paralysis compared with administration of the vehicle alone (p<0.01). Infiltration of ED1 macrophages and CD4 T cells into spinal cords occurred both in the absence and presence of melatonin treatment, but melatonin-treated rats had less spinal cord infiltration of inflammatory cells than did the control group. ICAM-1 immunoreactivity in the blood vessels of EAE lesions was decreased in melatonin-treated rats compared to vehicle-treated rats. These findings suggest that exogenous melatonin ameliorates EAE via a mechanism involving reduced expression of ICAM-1 and lymphocyte function associated antigen-1a in autoimmune target organs.
Animals ; Encephalomyelitis, Autoimmune, Experimental/*immunology/prevention & control ; Female ; Immunohistochemistry ; Intercellular Adhesion Molecule-1/analysis/*immunology ; Male ; Melatonin/administration & dosage/*physiology ; Rats ; Rats, Inbred Lew ; Spinal Cord/chemistry/pathology

OBJECTIVETo investigate the effects of complement inhibiting component of Ephedra sinica on immunological inflammation following acute spinal cord injury (SCI) in rats.

METHODSThe complement inhibiting component of Ephedra sinica was isolated by multiple precipitation steps and thin layer chromatography, and then the activity was analyzed. Fifty healthy SD rats were selected and randomly divided into the control group and the experimental group, 25 in each group. Induction of SCI was performed following a modified Allen's weight-drop method. The complement inhibiting component from Ephedra sinica (15 mg/kg) dissolving in 5 mL normal saline was immediately administered by gastrogavage after SCI, once daily. Equal volume of normal saline was administered to rats in the control group by gastrogavage. Hematoxylin and eosin (H&E) staining and C3 immunohistochemical staining were performed in SCI tissue at 12 h, day 1, 3, 7, and 14 after SCI. C3 positive expressions and myeloperoxidase (MPO) activity were assessed. Intercellular adhesion molecule-1 (ICAM-1) mRNA expression level was evaluated by Real-time PCR technique.

RESULTSC3 positive expression, MPO activity, and ICAM-1 mRNA level were significantly weaker in the Ephedra sinica group than in the control group at all time points (12 h, day 1, day 3, day 7, and day 14 after SCI) (P < 0.01, P < 0.05).

CONCLUSIONSThere existed complement system activation following acute SCI. The complement inhibiting component of Ephedra sinica significantly reduced immunological inflammation after SCI, and played an important role in secondary SCI.

Animals ; Complement Activation ; drug effects ; immunology ; Complement Inactivating Agents ; pharmacology ; Ephedra sinica ; chemistry ; Inflammation ; immunology ; Rats ; Rats, Sprague-Dawley ; Spinal Cord Injuries ; immunology ; metabolism ; pathology

Acute spinal cord injury (SCI) is two-step process that first involves the primary mechanical injury and then the secondary injury is induced by various biochemical reactions. Apoptosis is one of secondary SCI mechanisms and it is thought to play an important role for the delayed neuronal injury. The enhanced formation of nitric oxide (NO) via inducible nitric oxide synthase (iNOS) has been implicated in the pathogenesis of apoptosis in SCI. The level of .iNOS mRNA peaked at 6 hr after SCI and it declined until 72 hr after SCI in a rat model. Double-immunofluorescence staining revealed that iNOS positive cells were stained for ED-1, synaptophysin, GFAP, and oligodendrocyte marker. The terminal deoxynucleotidyl-transferase-mediated dUDP-biotin nick end-labeling (TUNEL) positive cell count was higher for the 72 hr post-SCI group than for the 24 hr post-SCI group. This cell count was also higher going in the caudal direction than in the rostral direction from the epicenter, and especially for the 72 hr group. Treatment with a selective iNOS inhibitor resulted in the reduction of TUNEL-positive cells at the lesion site. These findings suggest that nitric oxide generated by the iNOS of macrophages, neurons, oligodentrocytes, and astrocytes plays an important role for the acute secondary SCI that results from apoptotic cell death.
Analysis of Variance ; Animals ; Apoptosis ; Comparative Study ; Glial Fibrillary Acidic Protein/analysis ; In Situ Nick-End Labeling ; Microscopy, Fluorescence ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Sprague-Dawley ; Research Support, Non-U.S. Gov't ; Reverse Transcriptase Polymerase Chain Reaction ; Spinal Cord/chemistry/enzymology/pathology ; Spinal Cord Injuries/*enzymology/pathology/physiopathology ; Time Factors