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ORIGINAL ARTICLES
Published online: 2019-04-03
Submitted: 2019-02-20
Accepted: 2019-03-13
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Neuroprotective effects of allopurinol on spinal cord injury in rats: a biochemical and immunohistochemical study

Murat Baloğlu, Ebru Gökalp Özkorkmaz
DOI: 10.5603/FM.a2019.0036
·
Pubmed: 30949995

open access

Ahead of Print
ORIGINAL ARTICLES
Published online: 2019-04-03
Submitted: 2019-02-20
Accepted: 2019-03-13

Abstract

Lesion in spinal cord causes a cascade of events such as the apoptosis of neurons and eventually, neurological dysfunction.  Neurologic damage developing after acute spinal cord injury is also related with necrosis and free radical formation. Allopurinol a xanthine oxidase inhibitor, was shown to have protective effects in several studies. B-cell lymphoma 2 (Bcl-2) family proteins regulate apoptosis. Apoptosis causes the death of neuronal cells, particularly neurons and oligodendrocytes in the spinal cord after lesion. Glial fibrillary acidic protein (GFAP) takes part in astrocyte and neuronal interconnection and synaptic transmission. Male Sprague Dawley rats (n:30) were divided as control, trauma, and trauma + allopurinol (i.p., 50 mg/kg of body weight) groups. Animals were applied a surgical procedure causing spinal cord injury and treated for 7 days then sacrified under anesthesia. The spinal cords were dissected, measurements of myeloperoxidase, malondialdehyde and glutathione were performed, remaining parts were fixed in 10% formaldehyde solution for histological and immunohistochemical evaluations. Biochemical results exhibited an increase in myeloperoxidase levels in trauma group but a decrease in the allopurinol treatment group similar to malondialdehyde levels. Degenerative changes in multipolar and bipolar neurons together with apoptotic changes in some glial cells were observed in the trauma group whereas, mild degenerative changes were observed after allopurinol treatment. In the trauma group, negative GFAP expression in multipolar ve bipolar neuronal processes with a reduction in glial processes around blood vessels and positive GFAP expression were observed but, a regular and parallel positive GFAP expression of glial processes around blood vessels in the allopurinol treated group was apparent. Trauma group depicted a positive Bcl-2 expression in glial cells and in motor and bipolar neurons. On the contrary, negative Bcl-2 expression was noticed in the trauma + allopurinol group.  This study is of importance to understand the effects of allopurinol in preventing degenerative changes in nerve and glial cells related to spinal cord injuries.

Abstract

Lesion in spinal cord causes a cascade of events such as the apoptosis of neurons and eventually, neurological dysfunction.  Neurologic damage developing after acute spinal cord injury is also related with necrosis and free radical formation. Allopurinol a xanthine oxidase inhibitor, was shown to have protective effects in several studies. B-cell lymphoma 2 (Bcl-2) family proteins regulate apoptosis. Apoptosis causes the death of neuronal cells, particularly neurons and oligodendrocytes in the spinal cord after lesion. Glial fibrillary acidic protein (GFAP) takes part in astrocyte and neuronal interconnection and synaptic transmission. Male Sprague Dawley rats (n:30) were divided as control, trauma, and trauma + allopurinol (i.p., 50 mg/kg of body weight) groups. Animals were applied a surgical procedure causing spinal cord injury and treated for 7 days then sacrified under anesthesia. The spinal cords were dissected, measurements of myeloperoxidase, malondialdehyde and glutathione were performed, remaining parts were fixed in 10% formaldehyde solution for histological and immunohistochemical evaluations. Biochemical results exhibited an increase in myeloperoxidase levels in trauma group but a decrease in the allopurinol treatment group similar to malondialdehyde levels. Degenerative changes in multipolar and bipolar neurons together with apoptotic changes in some glial cells were observed in the trauma group whereas, mild degenerative changes were observed after allopurinol treatment. In the trauma group, negative GFAP expression in multipolar ve bipolar neuronal processes with a reduction in glial processes around blood vessels and positive GFAP expression were observed but, a regular and parallel positive GFAP expression of glial processes around blood vessels in the allopurinol treated group was apparent. Trauma group depicted a positive Bcl-2 expression in glial cells and in motor and bipolar neurons. On the contrary, negative Bcl-2 expression was noticed in the trauma + allopurinol group.  This study is of importance to understand the effects of allopurinol in preventing degenerative changes in nerve and glial cells related to spinal cord injuries.

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Keywords

allopurinol, GFAP, Bcl-2, spinal cord injury, rat

About this article
Title

Neuroprotective effects of allopurinol on spinal cord injury in rats: a biochemical and immunohistochemical study

Journal

Folia Morphologica

Issue

Ahead of Print

Published online

2019-04-03

DOI

10.5603/FM.a2019.0036

Pubmed

30949995

Keywords

allopurinol
GFAP
Bcl-2
spinal cord injury
rat

Authors

Murat Baloğlu
Ebru Gökalp Özkorkmaz

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