Therapeutic effect of vitamin D-3 in a rat diffuse axonal injury model

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Malcok U., SENGUL G., KADIOGLU H., AYDIN I.

JOURNAL OF INTERNATIONAL MEDICAL RESEARCH, cilt.33, sa.1, ss.90-95, 2005 (SCI-Expanded)

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 33 Sayı: 1
  • Basım Tarihi: 2005
  • Doi Numarası: 10.1177/147323000503300109
  • Dergi Adı: JOURNAL OF INTERNATIONAL MEDICAL RESEARCH
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.90-95
  • Anahtar Kelimeler: vitamin D-3, diffuse axonal injury, rat, NITRIC-OXIDE SYNTHASE, GLUTAMYL-TRANSPEPTIDASE ACTIVITY, GROWTH-FACTOR SYNTHESIS, 1,25-DIHYDROXYVITAMIN D-3, NEUROTROPHIC FACTOR, NEUROBLASTOMA-CELLS, NERVOUS-SYSTEM, BRAIN-INJURY, EXPRESSION, CALCIUM
  • Çanakkale Onsekiz Mart Üniversitesi Adresli: Hayır

Özet

We investigated the therapeutic effect of vitamin D-3 in a rat diffuse axonal injury model. A total of 60 male Sprague-Dawley rats weighing 175 - 200 g were anaesthetized and subjected to head trauma using Marmarou's impact-acceleration model. The rats were then separated into two groups; one group was treated with vitamin D-3 and the other with saline for up to 4 days after the head trauma. Rats from both groups were killed 1, 3 or 8 days post-injury. The brains were examined histopathologically and scored according to the level of neuronal, vascular and axonal damage. There were no significant differences between the groups after 1 or 3 days, but evaluation after 8 days revealed a significant improvement in the group treated with vitamin D-3. Our data indicate that vitamin D-3 has a beneficial effect in diffuse axonal injury and may be useful in the management of this condition.

We investigated the therapeutic effect of
vitamin D3 in a rat diffuse axonal injury
model. A total of 60 male Sprague–Dawley
rats weighing 175 – 200 g were
anaesthetized and subjected to head
trauma using Marmarou’s impactacceleration
model. The rats were then
separated into two groups; one group was
treated with vitamin D3 and the other
with saline for up to 4 days after the head
trauma. Rats from both groups were killed
1, 3 or 8 days post-injury. The brains were
examined histopathologically and scored
according to the level of neuronal, vascular
and axonal damage. There were no
significant differences between the groups
after 1 or 3 days, but evaluation after 8 days
revealed a significant improvement in the
group treated with vitamin D3. Our data
indicate that vitamin D3 has a beneficial
effect in diffuse axonal injury and may be
useful in the management of this condition.