Abstract
Hericium erinaceus, an edible and medicinal mushroom, displays various pharmacological activities in the prevention of dementia in conditions such as Parkinson’s and Alzheimer’s disease. The present study explored the neuroprotective effects of H. erinaceus mycelium polysaccharide-enriched aqueous extract (HE) on an l-glutamic acid (l-Glu)-induced differentiated PC12 (DPC12) cellular apoptosis model and an AlCl3 combined with d-galactose-induced Alzheimer’s disease mouse model. The data revealed that HE successfully induced PC12 cell differentiation. A 3 h HE incubation at doses of 50 and 100 µg/mL before 25 mM of l-Glu effectively reversed the reduction of cell viability and the enhancement of the nuclear apoptosis rate in DPC12 cells. Compared with l-Glu-damaged cells, in PC12 cells, HE suppressed intracellular reactive oxygen species accumulation, blocked Ca2+ overload and prevented mitochondrial membrane potential (MMP) depolarization. In the Alzheimer’s disease mouse model, HE administration enhanced the horizontal and vertical movements in the autonomic activity test, improved the endurance time in the rotarod test, and decreased the escape latency time in the water maze test. It also improved the central cholinergic system function in the Alzheimer’s mice, demonstrated by the fact that it dose-dependently enhanced the acetylcholine (Ach) and choline acetyltransferase (ChAT) concentrations in both the serum and the hypothalamus. Our findings provide experimental evidence that HE may provide neuroprotective candidates for treating or preventing neurodegenerative diseases.
Highlights
Chronic progressive degenerative damage to the central nervous system can cause neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), both of which have drawn the attention of researchers due to their devastating nature and limited therapeutic options [1]
In the mitochondria-mediated apoptotic process, the overload of intracellular calcium produces large amounts of reactive oxygen species (ROS) [6], which promotes the opening of mitochondrial permeability transition pores, prompting the dissipation of mitochondrial membrane potential (MMP) [7]
The robust neuroprotective effect of HE is associated with its suppression of ROS accumulation and the Ca2+ overload caused by L-Glu
Summary
Chronic progressive degenerative damage to the central nervous system can cause neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), both of which have drawn the attention of researchers due to their devastating nature and limited therapeutic options [1]. AD, an irreversible degenerative disease and the main cause of dementia, affects 60%–65% of people worldwide and frequently occurs among the elderly [2]. The pathomechanisms of neurodegenerative diseases remain largely unknown, hypotheses featuring neuronal apoptosis has emerged as an attractive theory supported by observations of apoptotic cells in affected brain regions [4]. In the mitochondria-mediated apoptotic process, the overload of intracellular calcium produces large amounts of reactive oxygen species (ROS) [6], which promotes the opening of mitochondrial permeability transition pores (mPTPs), prompting the dissipation of mitochondrial membrane potential (MMP) [7]. Functional and structural damage induced by AD in brain tissues results in energy deficiency, increased ROS, and neuronal death [8]
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