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Rutin inhibits amylin-induced neurocytotoxicity and oxidative stress.
- Source :
-
Food & function [Food Funct] 2015 Oct; Vol. 6 (10), pp. 3296-306. - Publication Year :
- 2015
-
Abstract
- Recent evidence showed that amylin deposition is not only found in the pancreas in type 2 diabetes mellitus (T2DM) patients, but also in other peripheral organs, such as kidneys, heart and brain. Circulating amylin oligomers that cross the blood-brain barrier and accumulate in the brain may be an important contributor to diabetic cerebral injury and neurodegeneration. Moreover, increasing epidemiological studies indicate that there is a significant association between T2DM and Alzheimer's disease (AD). Amylin and β-amyloid (Aβ) may share common pathophysiology and show strikingly similar neurotoxicity profiles in the brain. To explore the potential effects of rutin on AD, we here investigated the effect of rutin on amylin aggregation by thioflavin T dyeing, evaluated the effect of rutin on amylin-induced neurocytotoxicity by the MTT assay, and assessed oxidative stress, as well as the generation of nitric oxide (NO) and pro-inflammatory cytokines in neuronal cells. Our results showed that the flavonoid antioxidant rutin inhibited amylin-induced neurocytotoxicity, decreased the production of reactive oxygen species (ROS), NO, glutathione disulfide (GSSG), malondialdehyde (MDA) and pro-inflammatory cytokines TNF-α and IL-1β, attenuated mitochondrial damage and increased the GSH/GSSG ratio. These protective effects of rutin may have resulted from its ability to inhibit amylin aggregation, enhance the antioxidant enzyme activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) and reduce inducible nitric oxide synthase (iNOS) activity. These in vitro results indicate that rutin is a promising natural product for protecting neuronal cells from amylin-induced neurotoxicity and oxidative stress, and rutin administration could be a feasible therapeutic strategy for preventing AD development and protecting the aging brain or slowing neurodegenerative processes.
- Subjects :
- Alzheimer Disease drug therapy
Antioxidants pharmacology
Blood-Brain Barrier
Catalase metabolism
Diabetes Mellitus, Type 2 drug therapy
Glutathione Disulfide metabolism
Glutathione Peroxidase metabolism
Humans
Interleukin-1beta metabolism
Malondialdehyde metabolism
Neurons cytology
Neurons metabolism
Nitric Oxide metabolism
Nitric Oxide Synthase Type II genetics
Nitric Oxide Synthase Type II metabolism
Protective Agents pharmacology
Reactive Oxygen Species metabolism
Superoxide Dismutase metabolism
Tumor Necrosis Factor-alpha metabolism
Islet Amyloid Polypeptide toxicity
Neurons drug effects
Oxidative Stress drug effects
Rutin pharmacology
Subjects
Details
- Language :
- English
- ISSN :
- 2042-650X
- Volume :
- 6
- Issue :
- 10
- Database :
- MEDLINE
- Journal :
- Food & function
- Publication Type :
- Academic Journal
- Accession number :
- 26242245
- Full Text :
- https://doi.org/10.1039/c5fo00500k