In:
PLOS ONE, Public Library of Science (PLoS), Vol. 17, No. 6 ( 2022-6-29), p. e0270123-
Abstract:
Aging-induced memory impairment is closely associated with oxidative stress. D-Galactose (D-gal) evokes severe oxidative stress and mimics normal aging in animals. Curcumin, a natural flavonoid, has potent antioxidant and anti-aging properties. There are several proteins like glutathione S-transferase A1 (GSTA1), glutathione S-transferase omega-1 (GSTO1), kelch-like ECH-associated protein 1 (KEAP1), beta-secretase 1 (BACE1), and amine oxidase [flavin-containing] A (MAOA) are commonly involved in oxidative stress and aging. This study aimed to investigate the interaction of curcumin to these proteins and their subsequent effect on aging-associated memory impairment in two robust animal models: D-Gal and normal aged (NA) mice. The aging mice model was developed by administering D-gal intraperitoneally (i.p). Mice (n = 64) were divided into the eight groups (8 mice in each group): Vehicle, Curcumin-Control, D-gal (100mg/kg; i.p), Curcumin + D-gal, Astaxanthin (Ast) + D-gal, Normal Aged (NA), Curcumin (30mg/kg Orally) + NA, Ast (20mg/kg Orally) + NA. Retention and freezing memories were assessed by passive avoidance (PA) and contextual fear conditioning (CFC). Molecular docking was performed to predict curcumin binding with potential molecular targets. Curcumin significantly increased retention time (p 〈 0.05) and freezing response (p 〈 0.05) in PA and CFC, respectively. Curcumin profoundly ameliorated the levels of glutathione, superoxide dismutase, catalase, advanced oxidation protein products, nitric oxide, and lipid peroxidation in mice hippocampi. In silico studies revealed favorable binding energies of curcumin with GSTA1, GSTO1, KEAP1, BACE1, and MAOA. Curcumin improves retention and freezing memory in D-gal and nature-induced aging mice. Curcumin ameliorates the levels of oxidative stress biomarkers in mice. Anti-aging effects of curcumin could be attributed to, at least partially, the upregulation of antioxidant enzymes through binding with GSTA1, GSTO1, KEAP1, and inhibition of oxidative damage through binding with BACE1 and MAOA.
Type of Medium:
Online Resource
ISSN:
1932-6203
DOI:
10.1371/journal.pone.0270123
DOI:
10.1371/journal.pone.0270123.g001
DOI:
10.1371/journal.pone.0270123.g002
DOI:
10.1371/journal.pone.0270123.g003
DOI:
10.1371/journal.pone.0270123.g004
DOI:
10.1371/journal.pone.0270123.g005
DOI:
10.1371/journal.pone.0270123.g006
DOI:
10.1371/journal.pone.0270123.g007
DOI:
10.1371/journal.pone.0270123.g008
DOI:
10.1371/journal.pone.0270123.g009
DOI:
10.1371/journal.pone.0270123.g010
DOI:
10.1371/journal.pone.0270123.g011
DOI:
10.1371/journal.pone.0270123.g012
DOI:
10.1371/journal.pone.0270123.g013
DOI:
10.1371/journal.pone.0270123.t001
DOI:
10.1371/journal.pone.0270123.t002
DOI:
10.1371/journal.pone.0270123.s001
DOI:
10.1371/journal.pone.0270123.s002
DOI:
10.1371/journal.pone.0270123.s003
DOI:
10.1371/journal.pone.0270123.r001
DOI:
10.1371/journal.pone.0270123.r002
DOI:
10.1371/journal.pone.0270123.r003
DOI:
10.1371/journal.pone.0270123.r004
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2022
detail.hit.zdb_id:
2267670-3
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