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Dietary supplementation of pomegranate reduces the brain oxidative stress in transgenic tg2576 mouse model of Alzheimer disease (1025.5)
Author(s) -
Subash Selvaraju,
Essa Musthafa,
Guillemin Gilles,
AlAdawi Samir,
AlAsmi Abdullah,
Vaishnav Ragini
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1025.5
Subject(s) - oxidative stress , antioxidant , neuroprotection , catalase , lipid peroxidation , glutathione , chemistry , polyphenol , biochemistry , oxidative phosphorylation , transgene , pharmacology , medicine , enzyme , biology , gene
Oxidative stress may play a key role in Alzheimer's disease (AD) neuropathology. Pomegranates contain very high levels of antioxidant polyphenolic substances as compared to other fruits and vegetables. Polyphenols have been shown to be neuroprotective in different model systems. Here, the effects of the antioxidant, pomegranate fruit grown in Oman were tested on the Tg2576 AD mouse model. The four month old double Swedish APP mutation (APPsw/Tg2576) mice were fed an 4% pomegranate or control diet for 15 months and then assessed for the influence of diet on oxidative stress. Significant increase in oxidative stress in terms of enhanced levels of lipid peroxidation and protein carbonyls with concomitant decrease in activity of antioxidant enzymes was observed in control diet treated Tg2576 mice. 4% pomegranate supplementation attenuated oxidative damage, as evident by decreased LPO and protein carbonyl levels and restoration in activities of the antioxidant enzymes (SOD, catalase, GPx, GSH & GST). The activity of membrane bound enzymes (Na+ K+ ATPase and AChE) was altered in control diet treated Tg2576 mice brain regions and 4% pomegranate supplementation was able to restore the activity of enzymes to comparable values observed in controls. The results suggest 4% pomegranate in the diet might be beneficial for the treatment of AD associated oxidative stress. This work was supported by a research grant from The Research Council, Oman (RC/AGR/FOOD/11/01). Grant Funding Source : Supported by a research grant from The Research Council, Oman (RC/AGR/FOOD/11/01).