Effect of simvastatin on memory disorders and Hippocampal cell death in the model of the fetal alcoholic syndrome in male rats

Exposure to ethanol as a neurotratogen in the developmental period has destructive effects on the central nervous system and causes neurological disorders in adulthood. These disorders are associated with apoptosis in areas of the brain such as the hippocampus, by activating the oxidative-inflammatory cascade and high levels of nerve degeneration. Simvastatin, used as a drug to treat hypercholesterolemia, can cross the blood-brain barrier and its neuroprotective effects have been confirmed in several diseases of the nervous system. This study aimed to evaluate the protective activities of simvastatin on memory disorders and nerve cell necrosis in the rat hippocampus by postnatal alcohol exposure.

Male rat infants received 5.27 g / kg milk powder soluble ethanol on days 2-10 after birth by gavage. They also received 10 and 20 mg/kg of simvastatin on days 2-10 after birth subcutaneously. Cognitive memory abnormalities were assessed 36 days after birth by the new object detection and then, the number of necrotic cells was assessed by nissl staining.

Behavioral data showed that in the groups treated with simvastatin, the new object recognition memory increased compared to the ethanol group (P<0.01). In addition, in the ethanol group, an increase in cell death was observed in the CA1 region of the hippocampus, and treatment with simvastatin showed a significant decrease in the number of necrotic cells (P<0.01).

This study showed that simvastatin has a protective effect on alcohol-related neurological defects, although more research is needed in the future.