Amyloid  protein (A) elicits a toxic effect on neurons in vitro and in vivo. In present study we attempt to elucidate the mechanism by which A confers its neurotoxicity. The neuroprotective effects of phytoestrogens on A-mediated toxicity were also investigated. Cortical neurons treated with 5 M A-(25-35) for 40 h decreased the cell viability by 45.5 ؎ 4.6% concomitant with the appearance of apoptotic morphology. 50 M kaempferol and apigenin decreased the A-induced cell death by 81.5 ؎ 9.4% and 49.2 ؎ 9.9%, respectively. A increased the activity of caspase 3 by 10.6-fold and to a lesser extent for caspase 2, 8, and 9. The A-induced activation of caspase 3 and release of cytochrome c showed a biphasic pattern. Apigenin abrogated A-induced cytochrome c release, and the activation of caspase cascade. Kaempferol showed a similar effect but to a less extent. Kaempferol was also capable of eliminating A-induced accumulation of reactive oxygen species. These two events accounted for the remarkable effect of kaempferol on neuroprotection. Quercetin and probucol did not affect the A-mediated neurotoxicity. However, they potentiated the protective effect of apigenin. Therefore, these results demonstrate that A elicited activation of caspase cascades and reactive oxygen species accumulation, thereby causing neuronal death. The blockade of caspase activation conferred the major neuroprotective effect of phytoestrogens. The antioxidative activity of phytoestrogens also modulated their neuroprotective effects on A-mediated toxicity.
Hericium erinaceus, an ideal culinary-medicinal mushroom, has become a well-established candidate in promoting positive brain and nerve health-related activities by inducing the nerve growth factor from its bioactive ingredient. Among its active compounds, only erinacine A has confirmed pharmacological actions in the central nervous system in rats. Hence, this review has summarized the available information on the neurohealth properties of H. erinaceus mycelia enriched with erinacines, which may contribute to further research on the therapeutic roles of these mycelia. The safety of this mushroom has also been discussed. Although it has been difficult to extrapolate the in vivo studies to clinical situations, preclinical studies have shown that there can be improvements in ischemic stroke, Parkinson's disease, Alzheimer's disease, and depression if H. erinaceus mycelia enriched with erinacines are included in daily meals.
BackgroundThe fruiting body of Hericium erinaceus has been demonstrated to possess anti-dementia activity in mouse model of Alzheimer’s disease and people with mild cognitive impairment. However, the therapeutic potential of Hericium erinaceus mycelia on Alzheimer’s disease remains unclear. In this study, the effects of erinacine A-enriched Hericium erinaceus mycelia (HE-My) on the pathological changes in APPswe/PS1dE9 transgenic mouse model of Alzheimer’s disease are studied.ResultsAfter a 30 day oral administration to 5 month-old female APPswe/PS1dE9 transgenic mice, we found that HE-My and its ethanol extracts (HE-Et) attenuated cerebral Aβ plaque burden. It’s worth noting that the attenuated portion of a plaque is the non-compact structure. The level of insulin-degrading enzyme was elevated by both HE-My and HE-Et in cerebral cortex. On the other hand, the number of plaque-activated microglia and astrocytes in cerebral cortex and hippocampus were diminished, the ratio of nerve growth factor (NGF) to NGF precursor (proNGF) was increased and hippocampal neurogenesis was promoted after these administrations. All the mentioned benefits of these administrations may therefore improve the declined activity of daily living skill in APPswe/PS1dE9 transgenic mice.ConclusionsThese results highlight the therapeutic potential of HE-My and HE-Et on Alzheimer’s disease. Therefore, the effective components of HE-My and HE-Et are worth to be developed to become a therapeutic drug for Alzheimer’s disease.
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