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Introduction: Exposure to high altitude results in redox imbalance
and decreased cognitive performance of soldiers posted at high altitude.


Objective: To
evaluate cognitive performance enhancement through aqueous extract of Ganoderma lucidum and establishing role
of Nrf2, a master redox switch under hypobaric hypoxia.

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Material and methods: To evaluate
spatial learning and memory for cognitive performance, rats were trained in Morris
water maze to reach the hidden escape platform from four different zones for 5
days. Probe trial was conducted with platform removed, after which animals were
exposed to hypobaric hypoxia in simulation chamber. Experimental rats were
supplemented orally with aqueous extract of Ganoderma
lucidum during stress. Post
stress, probe trial was taken to record escape latency and navigation plot. Animals
were thereafter sacrificed; blood-plasma was collected for measuring hematological
parameters, biochemical parameters and levels of biogenic amines. Hippocampus
was excised for the measurement of biogenic amines levels as well as oxidative
stress related protein markers. Whole perfused brain was cryo-sectioned for
staining and immunohistochemistry.


Results: Hypobaric hypoxia increased the escape latency and cumulative path-length but decreased
the time spent in target quadrant, which were ameliorated by treatment with aqueous
extract of Ganoderma lucidum. Oxidant-antioxidant
balance, biogenic amines and neurogenesis were found to be altered in hippocampus
and plasma of rats exposed to hypobaric hypoxia and such changes were prevented
with the treatment of extract. Increased proliferation of healthy neurons was
confirmed by CV staining. The expression of brain-derived neurotrophic factor
(BDNF) and cAMP response element-binding protein (CREB) was facilitated by extract
treatment. Further, Nrf2 and its dependent factors: EPO and HO1 were found to
be highly expressive.


Conclusion: These findings suggest that extract has potent
neuropharmacological effect under low oxygen conditions and its possible mechanism
by modulating Nrf2 dependent pathway. 

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