ArticleNeurosurgical review2025
Microscopic, stereological, and biochemical investigation of the effects of vitamin B12 on vascular changes in an experimental subarachnoid hemorrhage model in rats.
Article in Neurosurgical review, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Effects of colchicine on SAH-induced vascular damage in an experimental subarachnoid hemorrhage model.Turkish journal of medical sciences · 2026Article
- Erratum to "Effects of colchicine on SAH-induced vascular damage in an experimental subarachnoid hemorrhage model" [Turkish Journal of Medical Sciences 56 (2) 2026 597-607].Turkish journal of medical sciences · 2026Article
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Authors and funding
6 authors.
Funding
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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.
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