# Pre- and post-traumatic boric acid therapy prevents oxidative stress-mediated neuronal apoptosis in spinal cord injury

**Authors:** Turan Kandemir, Ibrahim Sogut, Zeki Serdar Ataizi, Betul Can, Aysegul Oglakci-Ilhan, Dilek Burukoglu-Donmez, Gungor Kanbak

PMC · DOI: 10.22038/ijbms.2024.81531.17649 · Iranian Journal of Basic Medical Sciences · 2025-01-01

## TL;DR

This study shows that boric acid, given before or after spinal cord injury in rats, reduces oxidative stress and prevents nerve cell death.

## Contribution

The novel finding is that pre- and post-traumatic boric acid application effectively mitigates oxidative stress and apoptosis in spinal cord injury.

## Key findings

- Boric acid reduced oxidative stress markers like MDA, TOS, and OSI after spinal cord injury.
- Boric acid application decreased apoptosis markers Cytc and Casp3 in injured spinal cord tissues.
- Histological damage, including cell and myelin damage, was reduced with boric acid treatment.

## Abstract

In our study, the neuroprotective efficacy of pre- and post-traumatic applications of boric acid (BA) in rats with experimentally induced spinal cord injury (SCI) was investigated.

The experimental animals were divided into four groups: control group (C), SCI group (SCI), BA-treated group before SCI (BA+SCI), and BA-treated group after SCI (SCI+BA). Forty-eight hours after SCI, biochemical levels of malondialdehyde (MDA), total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), and cytochrome c (Cytc) and caspase-3 (Casp3) expressions were measured in the spinal cord tissues and were examined histologically.

After SCI, oxidative stress markers, such as MDA, TOS, and OSI, and apoptosis markers Cytc and Casp3 showed an increase in levels compared to Group C. The oxidative stress markers that increased after SCI decreased with BA+SCI application, while Cytc level, one of the apoptosis markers that increased after SCI, decreased in both groups with BA application. Cell, myelin, ependymal damage, and hemorrhage levels increased after SCI compared to Group C. These histological markers increased after SCI and decreased after BA+SCI. BA was found to reduce SCI-induced oxidative stress and oxidative stress-induced apoptosis.

BA administered before SCI was shown to be more effective in protecting neural damage.

## Linked entities

- **Proteins:** CytC (mitochondrial cytochrome C), CASP3 (caspase 3)
- **Chemicals:** boric acid (PubChem CID 7628), malondialdehyde (PubChem CID 10964)
- **Diseases:** spinal cord injury (MONDO:0043797)
- **Species:** Rattus norvegicus (taxon 10116)

## Full-text entities

- **Genes:** CYCS (cytochrome c, somatic) [NCBI Gene 54205] {aka CYC, HCS, THC4}, CASP3 (caspase 3) [NCBI Gene 836] {aka CPP32, CPP32B, SCA-1}
- **Diseases:** SCI (MESH:D013119), hemorrhage (MESH:D006470), neuronal apoptosis (MESH:D065703), ependymal damage (MESH:D020263), neural damage (MESH:D015441)
- **Chemicals:** MDA (MESH:D008315), BA (MESH:C032688)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11831752/full.md

## References

49 references — full list in the complete paper: https://tomesphere.com/paper/PMC11831752/full.md

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Source: https://tomesphere.com/paper/PMC11831752