# Microscopic, stereological, and biochemical investigation of the effects of vitamin B12 on vascular changes in an experimental subarachnoid hemorrhage model in rats

## TL;DR

This study shows that vitamin B12 may help reduce brain blood vessel damage and inflammation in rats with subarachnoid hemorrhage.

## Contribution

The study demonstrates vitamin B12's potential to mitigate oxidative stress and vascular injury in an experimental SAH model.

## Key findings

- Vitamin B12 reduced oxidative stress markers like TOS and OSI in SAH rats.
- B12 treatment lowered inflammatory cytokines (IL-1β, IL-6, TNF-α) in the SAH group.
- Histopathology showed less arterial wall thickening in B12-treated SAH rats.

## Abstract

Spontaneous subarachnoid hemorrhage (SAH) is a severe neurological condition with significant morbidity and mortality. Cerebral vasospasm, a common complication of SAH, is a leading cause of delayed ischemic injury. Oxidative stress and inflammation are central to the pathophysiology of vasospasm. Vitamin B12, a water-soluble vitamin with antioxidant and anti-inflammatory properties, has shown potential neuroprotective effects in experimental models. This study aimed to investigate the effects of vitamin B12 on vascular changes, oxidative stress, and inflammatory markers in an experimental rat model of SAH. Eighteen Sprague Dawley rats were divided into three groups: a control group, an SAH group, and an SAH + B12 group. SAH was induced by injecting autologous blood into the cisterna magna. The SAH + B12 group received intraperitoneal B12 (15 mcg/kg) at 1 and 24 h post-SAH. Biochemical parameters, including total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), and inflammatory cytokines (IL-1β, IL-6, TNF-α), were analyzed. Histopathological evaluation of the basilar artery was performed, measuring arterial diameter and wall thickness. The SAH group exhibited significant elevations in TOS, OSI, IL-1β, IL-6, and TNF-α levels, along with decreased TAS, indicating heightened oxidative stress and inflammation. The SAH + B12 group showed significant reductions in TOS, OSI, and inflammatory cytokines compared to the SAH group (p < 0.05), alongside improved TAS levels. Histopathological findings demonstrated reduced arterial wall thickening and preserved lumen diameter in the SAH + B12 group compared to the untreated SAH group. Although the differences in arterial diameter and wall thickness were not statistically significant, the findings suggest that B12 may mitigate SAH-induced vascular injury by reducing oxidative stress and inflammation. These results highlight B12's potential as a therapeutic agent for SAH-related vasospasm. Further studies are needed to validate these findings in larger populations and clinical settings.