Chestnut ‘castanea sativa mill.’ honey potential in preventing memory decline on alzheimer’s disease model mice: in vitro enzyme activities, behavioural, memorial and histopathological studies

Abstract

Abstract The primary purpose of this research is to investigate, both in vitro and in vivo studies, whether Chestnut 'Castanea sativa Mill.' Honey consumption, can counteract the neurodegeneration occurring in Alzheimer's model mice brains caused by aluminium chloride combined with D-galactose. Within the scope of in vitro studies. The antioxidant activity of chestnut honey at a non-toxic concentration was then evaluated by DPPH and CUPRAC methods, indicating its radical scavenging and copper (II) ion reduction abilities, respectively. Finally, the modified Ellman method was used to measure its anti-acetylcholinesterase activity. For the in vivo studies, two chestnut honey doses were used, 150 mg/kg and 300mg/kg. As for the neurodegeneration, it was induced by Aluminium chloride at 100 mg/kg combined with D-galactose at 120 mg/kg. Following the neurological tests, the brain were subjected to histopathological study. The dose of chestnut honey, which has no effect on fibroblast cell growth following the 24-hour treatment was detected as 0.25% -w/v-, this dose was used for further in vitro assays. DPPH scavenging activity of the honey was 10.98 ± 1.20 g/mL -IC50-, while CUPRAC value was 0.57 ± 0.27 mM TEAC/g. The neurological tests, reported significant positive improvement in learning ability, these results were confirmed by the histopathological findings, in which the tissues section taken from the brain showed that, the honey markedly reduced hippocampal atrophy and neuronal loss. The results suggests that Chestnut honey acceptable daily-inake can reduce the burden of Alzheimer's disease, by preventingmemory impairment and brain alteration.