title: [Expression of neurotrophin and IL-1 beta mRNAs following spinal cord injury and the effects of methylprednisolone treatment].
abstract: Glucocorticoid has been clinically used for the treatment of acute spinal cord injury (SCI) to enhance the neurological recovery, but the relevance of the use of steroid is not fully discussed. Neurotrophins play important roles in normal development of central and peripheral nervous system. It is reported that traumatic insults to the brain alter the expression of these neurotrophins. These responses are considered to trigger a cascade of cellular protection and repair. First, we investigated the temporal and spatial expression patterns of neurotrophin and IL-1 beta mRNAs in the area of spinal cord lesion. Second, we examined if methylprednisolone (MP) affects the expression of these genes in SCI. Male Sprague-Dawley rats (250-300 gms) were laminectomized at T10. Spinal cord was crushed by clipping (holding force 60 gms, 1 sec). Rats were killed at 1, 6, 12, 24 h, and 72 h after the injury and the spinal cord was rapidly removed and frozen sections were cut. Second, the other group of rats were treated with MP (165 mg/kg) just after SCI and sacrificed at 6 h. The levels of neurotrophins and IL-1 beta mRNAs were evaluated by in situ hybridization histochemistry. IL-1 beta mRNA level was elevated at 1 h and 6 h and attenuated at 12 h. The increased level of BDNF and NT3 mRNAs were first observed at 6 h and the labeling was enhanced at 24 h and 72 h. In MP treated group, the levels of IL-1 beta, BDNF and NT3 mRNAs were attenuated compared with those of MP-untreated SCI group. Steroid hormone therapy diminishes the post-traumatic inflammatory cascades which produce edema and swelling and worsen neuronal injury. However, glucocorticoid may hinder the endogenous repair mechanism. Our data show that MP depress the production of BDNF and NT3 following SCI, which might be disadvantageous to the survival of spinal neurons.
authors.affiliation: Dept. of Orthopedic Surgery, Wakayama Medical College, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Hayashi
authors.forename: T
authors.initials: T
authors.lastname: Ueyama
authors.forename: T
authors.initials: T
authors.lastname: Tamaki
authors.forename: E
authors.initials: E
authors.lastname: Senba
mesh_terms: D000818:Animals; D019208:Brain-Derived Neurotrophic Factor / Q000235:genetics; D005938:Glucocorticoids / Q000494:pharmacology* / Q000627:therapeutic use*; D007375:Interleukin-1 / Q000235:genetics*; D008297:Male; D008775:Methylprednisolone / Q000494:pharmacology* / Q000627:therapeutic use*; D009414:Nerve Growth Factors / Q000235:genetics*; D018696:Neuroprotective Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D020933:Neurotrophin 3; D012333:RNA, Messenger / Q000032:analysis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013119:Spinal Cord Injuries / Q000188:drug therapy* / Q000378:metabolism*
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D005938:Glucocorticoids; D007375:Interleukin-1; D009414:Nerve Growth Factors; D018696:Neuroprotective Agents; D020933:Neurotrophin 3; D012333:RNA, Messenger; D008775:Methylprednisolone