Folic Acid Supplementation Diminishes Diabetes Induced Neural Tube Defects by Recovering Impaired Embryo Gene Expression Through Its Antioxidant Activity

Abstract

Aimes: This study aimed to determine whether folic acid supplementation could decrease the neural tube defects (NTDs) in embryos caused by hyperglycemia and the mechanism is associated with its antioxidative activity. Study Design: Diabetic pregnancy model were made and folic acid, Vitamin E and control were given to mice. Then the neural tube defects rate, oxidative stress markers and embryos size were measured and were analyzed.  Methodology: We injected folic acid to diabetic mice to score NTDs rate, measured embryos size, assayed ROS scavenging enzymes and Pax3 expression and oxidative stress marker including malondiadehyde and H2O2 as well as the vitamin E controls. Results: Injection of folic acid during gestation could diminish neural tube defect rate of diabetic mice and recover the Pax3 expression inhibition which is similar to vitamin E, but no effect was observed on nondiabetic mice. Folic acid supplementation also normalized the embryos size, decreased oxidative stress level including malondiadehyde and H2O2 in diabetic mice and decreased the intracellular ROS of embryonic cells on day 8.5 induced by high glucose incubation in a dose-dependent manner. No effects were observed on ROS scavenging enzymes activity by folic acid supplementation. Conclusion: Overall, the conclusion is that folic acid supplementation could diminish NTDs induced by hyperglycemia, the mechanism is associated with its antioxidant activity which can reduce the oxidative stress and recover the inhibition of Pax3 expression.