According
to experimental and clinical findings, fetal brain development may be
interrupted by maternal alcohol consumption during pregnancy. Adult
hippocampal neurogenesis is thought to play a role in cognition function
(i.e. learning and memory). Recent evidence suggests that ethanol
administration causes major apoptotic neurodegeneration in many regions
of the rats’ developing brain during the synaptogenesis period. Based on
the recent studies, H2S improve learning and memory via
increased neurogenesis and antiapoptotic mechanisms in different animal
models. In this study, we aimed to evaluate the protective effects of
hydrogen sulfide on alcohol-induced memory impairment, hippocampus
neurogenesis and neuronal apoptosis in rat pups with postnatal ethanol
exposure.
Administration of ethanol to male rat pups
was performed through intragastric intubation on postnatal days 2-10.
The pups were administered 1 mg/kg of NaHS (H2S donor) on
postnatal days 2-10. For examining the spatial memory, Morris water maze
test was carried out 36 days after birth. Following the behavioral
test, immunohistochemical staining was performed to evaluate the
expression levels of BrdU, BDNF and Apoptotic cell death was detected by
TUNEL staining.
Hydrogen sulfide (H2S)
treatment could significantly improve spatial memory impairment (P<
0.05) and significantly increase the expression of BrdU and BDNF in
dentate gyrus area (P< 0.05). It also decreased positive TUNEL cells,
compared with the ethanol group (P< 0.01).
Based on the findings, H2S makes significant neuroprotective effects on Ethanol neurotoxicity due to its neurogenesis and anti-apoptotic activity.
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