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<p>Cerebral vasospasm is seen in 30–70% of subarachnoid hemorrhage (SAH) patients. The aim of the presented study was to investigate the effectiveness of vitamin E on vasospasm, oxidative stress, inflammatory response and apoptotic process in an experimental SAH rat model. Rats were randomly distributed into three separate groups. In SAH and VIT E groups, 0.2 mL of cerebrospinal fluid was withdrawn by cisterna magna puncture. It was replaced with an equal volume of non-heparinized autologous arterial blood. The VIT E group was injected with 100&#xa0;mg/kg vitamin E intraperitoneally at the 1st hour and 24th hour after SAH induction. All animals were euthanized 48&#xa0;h after SAH induction, and blood and brain tissue samples were collected. Basilar artery lumen diameter was found to increase in the VIT E group compared to the SAH group, but this increase was not statistically significant. Total antioxidant level (TAS), total thiol and natural thiol values were significantly higher in the VIT E group compared to the SAH group (<i>p</i> &lt; 0.001, <i>p</i> &lt; 0.01, <i>p</i> &lt; 0.001, respectively). In contrast, total oxidant level (TOS), oxidative stress index (OSI), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), hypoxia inducible factor 1 alpha and Cytokeratin 18-M65 values were significantly decreased (all <i>p</i> &lt; 0.001). In the experimental SAH model, vitamin E treatment has been shown to reduce the levels of TOS, IL-1β, TNF-α, and IL-6, have antioxidant and anti-inflammatory effects, partially stabilize thiol-disulfide homeostasis, and increase TAS levels. In conclusion, vitamin E is thought to contribute to the reduction of secondary damage after SAH by reducing oxidative stress and inflammation.</p>

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Vitamin E reduces vasospasm in a rat subarachnoid hemorrhage model

  • 期刊论文

  • 发表日期：

    2025年10月18日

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  • Cumaali Demirtas,
  • Eyüp Çetin,
  • Murat Yucel,
  • Cansu Sönmez,
  • Eray Metin Güler,
  • Hakan Beyaztaş,
  • Mehmet Yildirim

摘要

Cerebral vasospasm is seen in 30–70% of subarachnoid hemorrhage (SAH) patients. The aim of the presented study was to investigate the effectiveness of vitamin E on vasospasm, oxidative stress, inflammatory response and apoptotic process in an experimental SAH rat model. Rats were randomly distributed into three separate groups. In SAH and VIT E groups, 0.2 mL of cerebrospinal fluid was withdrawn by cisterna magna puncture. It was replaced with an equal volume of non-heparinized autologous arterial blood. The VIT E group was injected with 100 mg/kg vitamin E intraperitoneally at the 1st hour and 24th hour after SAH induction. All animals were euthanized 48 h after SAH induction, and blood and brain tissue samples were collected. Basilar artery lumen diameter was found to increase in the VIT E group compared to the SAH group, but this increase was not statistically significant. Total antioxidant level (TAS), total thiol and natural thiol values were significantly higher in the VIT E group compared to the SAH group (p < 0.001, p < 0.01, p < 0.001, respectively). In contrast, total oxidant level (TOS), oxidative stress index (OSI), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), hypoxia inducible factor 1 alpha and Cytokeratin 18-M65 values were significantly decreased (all p < 0.001). In the experimental SAH model, vitamin E treatment has been shown to reduce the levels of TOS, IL-1β, TNF-α, and IL-6, have antioxidant and anti-inflammatory effects, partially stabilize thiol-disulfide homeostasis, and increase TAS levels. In conclusion, vitamin E is thought to contribute to the reduction of secondary damage after SAH by reducing oxidative stress and inflammation.