Inadequate
oxygen availability at high altitude causes elevated oxidative stress, resulting in hippocampal neurodegeneration and memory impairment. Though oxidative stress is known to be a major cause of neurodegeneration in hypobaric
hypoxia, neuroprotective and ameliorative potential of
quercetin, a
flavonoid with strong
antioxidant properties in reversing hypobaric
hypoxia-induced memory impairment has not been studied. Four groups of male adult Sprague Dawley rats were exposed to hypobaric
hypoxia for 7 days in an animal
decompression chamber at an altitude of 7600 meters. Rats were supplemented with
quercetin orally by gavage during 7 days of hypoxic exposure. Spatial working memory was assessed by a Morris Water Maze before and after exposure to hypobaric
hypoxia. Changes in oxidative stress markers and apoptotic marker
caspase 3 expression in hippocampus were assessed. Histological assessment of neurodegeneration was performed by
cresyl violet and
fluoro Jade B staining. Our results showed that
quercetin supplementation during exposure to hypobaric
hypoxia decreased
reactive oxygen species levels and consequent lipid peroxidation in the hippocampus by elevating
antioxidant status and
free radical scavenging
enzyme system. There was reduction in
caspase 3 expression, and decrease in the number of pyknotic and
fluoro Jade B-positive neurons in hippocampus after
quercetin supplementation during hypoxic exposure. Behavioral studies showed that
quercetin reversed the hypobaric
hypoxia-induced memory impairment. These findings suggest that
quercetin provides neuroprotection to hippocampal neurons during exposure to hypobaric
hypoxia through antioxidative and anti-apoptotic mechanisms, and possesses promising therapeutic potential to ameliorate
hypoxia-induced memory dysfunction.