Abstracts

Rationale:
Prenatal stress increases the susceptibility of infants to seizures and is known to be associated with oxidative stress. Recent studies suggest that vitamin E has beneficial effects in various neurological diseases due to its antioxidant properties. In this study, we investigated the relationship between prenatal stress and vitamin E treatment on infantile spasms.
Method:
We used pregnant female Sprague Dawley rats and induced prenatal stress with an injection of betamethasone on G15. They were then treated orally with 200 mg/kg vitamin E or saline twice a day from G15-G21. On postnatal day 15, N-methyl-D-aspartate was administered to trigger spasms. The total number of spasms and latency to the first spasm were recorded. We also measured oxidative stress in the whole cortex through various biochemical assays.
Results:
As a result, we observed that rats treated with vitamin E while exposed to prenatal stress demonstrated reduced total number and frequency of spasms. Expression of glutamate decarboxylase 67 and K+/Cl- co-transporter were reduced after prenatal stress, which was recovered in the vitamin E treated group. Further, expression of calpain 2 was decreased, and various markers of oxidative stress were reduced in the vitamin E treated group.
Conclusion:
Our results provide evidence that vitamin E lowers oxidative stress and decreases seizure susceptibility in rat offspring exposed to prenatal stress. Considering the well-known safety profile of vitamin E, these results indicate its potential as a possible strategy to prevent seizures.
Funding:
:This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF), funded by the Ministry of Science, ICT, and Future Planning (2015R1C1A1A01052351 and NRF-2019R1F1A1041058).