Abstract
Alzheimer's disease (AD) is the most common neurodegenerative disease, affecting the elderly at a high incidence. AD is of unknown etiology and currently, no cure is available. Present medication is restricted to treating symptoms; thus, a need exists for the development of effective remedies. Medicinal plants constitute a large pool, from which active compounds of great pharmaceutical potential can be derived. Various Salvia spp. are considered as neuroprotective, and here, the ability of Salvia fruticosa (SF) to protect against toxic effects induced in an AD cell model was partly assessed. Two of AD's characteristic hallmarks are the presence of elevated oxidative stress levels and the cytotoxic aggregation of amyloid beta (Aβ) peptides. Thus, we obtained SF extracts in three different solvents of increasing polarity, consecutively, to evaluate (a) their antioxidant capacity with the employment of the free radical scavenging assay (DPPH•), of the ferric reducing ability of plasma assay (FRAP), and of the cellular reactive oxygen species assay (DCFDA) and (b) their neuroprotective properties against Aβ25–35-induced cell death with the use of an MTT assay. All three SF extracts showed a considerable antioxidant capacity, with the methanol (SFM) extract being the strongest. The results of the total phenolic and flavonoid contents (TPC and TFC) of the extracts and of the FRAP and the DCFDA assays showed a similar pattern. In addition, and most importantly, the dichloromethane (SFD) and the petroleum ether (SFP) extracts had an effect on Aβ toxicity, exhibiting a significant neuroprotective potential. To our knowledge, this is the first report of SF extracts demonstrating neuroprotective potential against Aβ toxicity. In combination with their antioxidant capacity, SF extracts may be beneficial in combating AD and other neurodegenerative diseases.
Highlights
Alzheimer’s disease (AD) is a progressive neurological disorder with a prevalence of 5% among individuals over 65 years old, increasing to 30% among those over 85 years old
One of the main contributing factors to AD’s progression is the presence of oxidative stress, i.e., a disturbance in the balance between oxidants and antioxidants, in favour of the oxidants. is phenomenon promotes the generation of damaging accumulates of reactive oxygen species (ROS), which contribute to the accumulation of the neurotoxic extracellular amyloid beta (Aβ) plaques in the brain. ese deposits further increase oxidative stress, causing more damage to the cells, especially to the neurons that are more vulnerable to the oxidants’ activity [2,3,4]
Radical scavenging activity expressed as EC50 ranged from 0.336 to 1.477 mg dry extract/mg DPPH
Summary
Alzheimer’s disease (AD) is a progressive neurological disorder with a prevalence of 5% among individuals over 65 years old, increasing to 30% among those over 85 years old. It is the commonest form of dementia, as well as the most prevalent neurodegenerative disorder, and is dramatically affecting cognitive and behavioural skills [1]. One of the main contributing factors to AD’s progression is the presence of oxidative stress, i.e., a disturbance in the balance between oxidants and antioxidants, in favour of the oxidants. There is no available cure for AD, and no significant progress on treatment has been documented in the past 2 decades.
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