Introduction: Exposure to high altitude results in redox imbalanceand decreased cognitive performance of soldiers posted at high altitude. Objective: Toevaluate cognitive performance enhancement through aqueous extract of Ganoderma lucidum and establishing roleof Nrf2, a master redox switch under hypobaric hypoxia. Material and methods: To evaluatespatial learning and memory for cognitive performance, rats were trained in Morriswater maze to reach the hidden escape platform from four different zones for 5days.
Probe trial was conducted with platform removed, after which animals wereexposed to hypobaric hypoxia in simulation chamber. Experimental rats weresupplemented orally with aqueous extract of Ganodermalucidum during stress. Poststress, probe trial was taken to record escape latency and navigation plot. Animalswere thereafter sacrificed; blood-plasma was collected for measuring hematologicalparameters, biochemical parameters and levels of biogenic amines. Hippocampuswas excised for the measurement of biogenic amines levels as well as oxidativestress related protein markers. Whole perfused brain was cryo-sectioned forstaining and immunohistochemistry.
Results: Hypobaric hypoxia increased the escape latency and cumulative path-length but decreasedthe time spent in target quadrant, which were ameliorated by treatment with aqueousextract of Ganoderma lucidum. Oxidant-antioxidantbalance, biogenic amines and neurogenesis were found to be altered in hippocampusand plasma of rats exposed to hypobaric hypoxia and such changes were preventedwith the treatment of extract. Increased proliferation of healthy neurons wasconfirmed by CV staining. The expression of brain-derived neurotrophic factor(BDNF) and cAMP response element-binding protein (CREB) was facilitated by extracttreatment. Further, Nrf2 and its dependent factors: EPO and HO1 were found tobe highly expressive.
Conclusion: These findings suggest that extract has potentneuropharmacological effect under low oxygen conditions and its possible mechanismby modulating Nrf2 dependent pathway.