Corticosteroids reduce glial fibrillary acidic protein expression in response to spinal cord injury in a fetal rat model of dysraphism.
BACKGROUND
Exposure of the spinal cord in myelomeningocele (MM) throughout gestation increases spinal injury. Astrocyte activation evidenced by glial fibrillary acidic proteins (GFAP) indicates the extent of injury. Corticosteroids modulate GFAP synthesis, but their effect in MM is unclear. The purpose of this study was to evaluate the GFAP expression in a fetal rat model of dysraphism and the effect of corticosteroid treatment on this marker and on clinical neurological disabilities.


METHODS
Dysraphism was surgically created in 2 groups of 48 rat fetuses; group 1: control, and group 2: treated with corticosteroid. Each group was subdivided into fetuses with surgically created MM, controls and shams on day 18.5 of gestation (term = 22 days). Fetuses were harvested on day 21.5, examined for evidence of neurological deficits, and the following clinical parameters were registered: kyphosis, tail deformities, leg deformities, leg paralysis or paresis and pain perception. The fetuses were fixed for GFAP immunostaining.


RESULTS
All fetuses with MM in group 1 presented neurological deficits and glial reactions with GFAP expression, as opposed to controls and shams. In group 2, corticosteroid treatment prevented some neurological deficits (18-25%), reducing glial response and GFAP expression.


CONCLUSIONS
Experimentally induced dysraphism in the rat fetus is related to glial response and increased GFAP expression in the spinal cord. Corticoid treatment clinically improved nerve injury in some fetuses. It reduced glial reaction and GFAP expression.
Melo-Filho
Antônio Aldo
AA
Division of Pediatric Surgery, Department of Surgery, Faculty of Medical Sciences, University of Campinas, UNICAMP, Campinas, Brazil.
Weber Guimarães Barreto
Maria
M
Capelli Nassr
Azize Cristina
AC
Rogério
Fábio
F
Langone
Francesco
F
Pereira
Luis Antonio Violin
LA
Sbragia
Lourenço
L
D000305:Adrenal Cortex Hormones / Q000494:pharmacology*; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism*; D005911:Gliosis / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D008297:Male; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000378:metabolism / Q000473:pathology; D013119:Spinal Cord Injuries / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D016135:Spinal Dysraphism / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology
D000305:Adrenal Cortex Hormones; D015415:Biomarkers; D005904:Glial Fibrillary Acidic Protein