The Effect of Obstatin on Stress, Anxiety, Necrosis Cell Death and Apoptosis in the Hippocampus Area in the Model of Fetal Alcohol Spectrum Disorders in Male Rats

Among the numerous consequences of prenatal alcohol exposure (PAE) is an increase in anxiety-like behavior that can prove debilitating to daily functioning. Clinical and experimental evidence has shown postnatal alcohol exposure causes inflammation in the hippocampus and reduced neurogenesis among other brain regions. This can occur during early growth due to the low levels of antioxidants in the brain can be harmful and dangerous. Obstatin is a newly discovered peptide with antiinflammatory, antioxidant activity, in various animal models.

Through intragastric intubation, ethanol (5.27 g/kg/day) was administered in male Wistar rat pups on postnatal days 2- 10 (third trimester in humans). The animals received obestatin (1 and 5 µg/kg, S.C.) on postnatal days 2-10. Thirty-six days after birth, the anexity test was performed using elevated plus maze test, and then. The level of necrotic and apoptosis cells death was determined via nissl and TUNEL staining after the behavioral test.

Obestatin significantly improved anxiety behavioral deficits (P<0.01), and obestatin treatment could significantly and decreased nissl and tunnel positive cells in the hippocampus of ethanol-exposed rat pups (P<0.01).

The result of this study shows that abstatin had a protective effect on neurodegenerative, alcohol-related behaviors, although further research is needed in the future.