Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder with an unclear cause. It appears that multiple factors participate in the process of neuronal damage including oxidative stress and accumulation of the protein amyloid β (Aβ) in the brain. The search for a treatment for this disorder is essential as current medications are limited to alleviating symptoms and palliative effects. The aim of this study is to investigate the effects of mint extracts on selected mechanisms implicated in the development of AD. To enable a thorough investigation of mechanisms, including effects on β-secretase (the enzyme that leads to the formation of Aβ), on Aβ aggregation, and on oxidative stress and apoptosis pathways, a neuronal cell model, SH-SY5Y cells, was selected. Six Mentha taxa were investigated for their in vitro β-secretase (BACE) and Aβ-aggregation inhibition activities. Moreover, their neuroprotective effects on H2O2-induced oxidative stress and apoptosis in SH-SY5Y cells were evaluated through caspase activity. Real-time PCR and Western blot analysis were carried out for the two most promising extracts to determine their effects on signalling pathways in SH-SY5Y cells. All mint extracts had strong BACE inhibition activity. M. requienii extracts showed excellent inhibition of Aβ-aggregation, while other extracts showed moderate inhibition. M. diemenica and M. requienii extracts lowered caspase activity. Exposure of SH-SY5Y cells to M. diemenica extracts resulted in a decrease in the expression of pro-apoptotic protein, Bax, and an elevation in the anti-apoptotic protein, Bcl-xL, potentially mediated by down-regulation of the ASK1-JNK pathway. These results indicate that mint extracts could prevent the formation of Aβ and also could prevent their aggregation if they had already formed. M. diemenica and M. requienii extracts have potential to suppress apoptosis at the cellular level. Hence, mint extracts could provide a source of efficacious compounds for a therapeutic approach for AD.
Highlights
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that is characterized by memory impairment and cognitive decline due to loss of neurons [1]
Results are presented as mean ± standard error (SE) (n =3)
All mint in the present study showed a strong BACE inhibition activity indicating their potential to prevent the extracts in the present study showed a strong BACE inhibition activity indicating their potential to formation of senile plaques
Summary
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that is characterized by memory impairment and cognitive decline due to loss of neurons [1]. Accumulation of amyloid β (Aβ) protein outside the neurons in the brain is believed to be the initial event of the disease [3]. AD brain is characterized by Aβ plaques and intraneuronal neurofibrillary tangles of hyperphosphorylated-tau [4]. This accumulation disrupts neuron–neuron communication and leads to neuronal death [1]. Secretase inhibitors were believed to delay the progression of AD through a reduction in the rate of Aβ generation [5]. These compounds have not shown efficacy in clinical trials [3]. It has been suggested that antioxidants could be beneficial in AD [7]
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