Abstract
Armillaria mellea, an edible fungus, exhibits various pharmacological activities, including antioxidant and antiapoptotic properties. However, the effects of A. mellea on Alzheimer's disease (AD) have not been systemically reported. The present study aimed to explore the protective effects of mycelium polysaccharides (AMPS) obtained from A. mellea, especially AMPSc via 70% ethanol precipitation in a L-glutamic acid- (L-Glu-) induced HT22 cell apoptosis model and an AlCl3 plus D-galactose- (D-gal-) induced AD mouse model. AMPSc significantly enhanced cell viability, suppressed nuclear apoptosis, inhibited intracellular reactive oxygen species accumulation, prevented caspase-3 activation, and restored mitochondrial membrane potential (MMP). In AD mice, AMPSc enhanced horizontal movements in an autonomic activity test, improved endurance times in a rotarod test, and decreased escape latency time in a water maze test. Furthermore, AMPSc reduced the apoptosis rate, amyloid beta (Aβ) deposition, oxidative damage, and p-Tau aggregations in the AD mouse hippocampus. The central cholinergic system functions in AD mice improved after a 4-week course of AMPSc administration, as indicated by enhanced acetylcholine (Ach) and choline acetyltransferase (ChAT) concentrations, and reduced acetylcholine esterase (AchE) levels in serum and hypothalamus. Our findings provide experimental evidence suggesting A. mellea as a neuroprotective candidate for treating or preventing neurodegenerative diseases.
Highlights
Devastating neurodegenerative disorders, such as Alzheimer’s disease (AD), are caused by neuronal loss and synapse degeneration
annexin V (AV)-propidium iodide (PI) staining revealed that whereas exposure to 25 mM L-Glu led to an apoptosis rate of 25% in HT22 cells, a 3 h preincubation with AMPSc led to a reduction in apoptosis of >14% (Figure 2(c))
Our present study successfully confirmed the neuroprotective effects of A. mellea mycelium polysaccharides (AMPS) in L-Glu-induced HT22 apoptotic cells and a chemically induced AD mouse model, as evidenced by the significant amelioration of nuclear and mitochondrial apoptosis
Summary
Devastating neurodegenerative disorders, such as Alzheimer’s disease (AD), are caused by neuronal loss and synapse degeneration. These disorders are clinically characterized by learning and memory decline, as well as cognitive deficits, and no cure is currently available [1]. Antioxidant therapies are being considered as new options for protecting neurons from the oxidative damage associated with AD. These antioxidants can scavenge free radicals but may reduce damage due to oxidative stress and maintain the cellular redox balance [6]
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