Vitamin E reduces vasospasm in a rat subarachnoid hemorrhage model

Area of Science:

• Neuroscience
• Biochemistry
• Pharmacology

Background:

• Cerebral vasospasm affects 30-70% of subarachnoid hemorrhage (SAH) patients.
• Oxidative stress, inflammation, and apoptosis are key contributors to secondary brain injury following SAH.

Purpose of the Study:

• To evaluate the efficacy of vitamin E in mitigating vasospasm, oxidative stress, inflammation, and apoptosis in an experimental SAH rat model.
• To assess the impact of vitamin E on biochemical markers of oxidative stress and inflammation.

Main Methods:

• SAH was induced in rats by cisterna magna puncture and replacement with autologous blood.
• The treatment group received intraperitoneal injections of vitamin E (100 mg/kg) at 1 and 24 hours post-SAH.
• Biochemical analyses were performed on blood and brain tissue samples collected 48 hours after SAH induction.

Main Results:

• Vitamin E treatment led to a significant increase in total antioxidant level (TAS), total thiol, and natural thiol values.
• Significant reductions were observed in total oxidant level (TOS), oxidative stress index (OSI), IL-1β, IL-6, TNF-α, and other markers.
• While basilar artery lumen diameter increased in the vitamin E group, the change was not statistically significant.

Conclusions:

• Vitamin E exhibits significant antioxidant and anti-inflammatory properties in the SAH rat model.
• It helps stabilize thiol-disulfide homeostasis and increases TAS levels.
• Vitamin E may play a role in reducing secondary damage after SAH by combating oxidative stress and inflammation.