In vitro assessment of selected Korean plants for antioxidant and antiacetylcholinesterase activities.
Λέξεις-κλειδιά
Αφηρημένη
BACKGROUND
Antiacetylcholinesterase (AChE) drugs have been a main therapeutic treatment for Alzheimer's disease because increased AChE levels play a key role in reducing neurotransmission.
OBJECTIVE
Extracts from 35 Korean plants were selected and screened for antioxidant and anti-cholinesterase activity to explore new sources derived from Korean natural resources that could be used as AD therapeutic agents.
METHODS
The antioxidant effect of extracts from 35 selected Korean plants was determined using two most common free radical scavenging assays using 1,1-diphenyl-2-picrylhydrazyl (DPPH) and 2,2'-azino-bis-3-ethylbenzthiazoline-6-sulphonic acid (ABTS). Additionally, the effect of extracts, identified as antioxidants, on acetylcholinesterase inhibition was assessed by an acetylcholinesterase assay kit.
RESULTS
Out of 36 extracts of 35 plants tested, Oenothera biennis L. (9.09 μg/mL), Saururus chinensis (Lour.) Baill. (9.52 μg/mL) and Betula platyphylla var. japonica (9.85 μg/mL) showed strong DPPH scavenging activity. Twelve other extracts also exerted moderate free radical scavenging activities with IC50 values ranging from 10 to 50 μg/mL. Antioxidant capacity detected by ABTS assay was only significant in O. biennis (23.40 μg/mL), while the other extracts were weak or unable to reduce the production of ABTS. Based on the antioxidant activities of these plant extracts, 19 extracts with IC50 values less than 100 μg/mL in DPPH assay were selected for further AChE inhibition assay. Among the extracts tested, the IC50 value for Prunella vulgaris var. lilacina NAKAI (18.83 μg/mL) in AChE inhibitory activity was the lowest, followed by O. biennis (20.09 μg/mL) and Pharbitis nil Chosy (22.79 μg/mL).
CONCLUSIONS
Considering complex multifactorial etiology of AD, the extracts of P. vulgaris var. lilacina (aerial part), O. biennis (seed) and P. nil (seed) may be safe and ideal candidates for future AD modifying therapies.
