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Metabolic Brain Disease

Erschienen in:

01.06.2015 | Research Article

Blueberry treatment decreased D-galactose-induced oxidative stress and brain damage in rats

verfasst von: Jale Çoban, Işın Doğan-Ekici, A. Fatih Aydın, Esra Betül-Kalaz, Semra Doğru-Abbasoğlu, Müjdat Uysal

Erschienen in: Metabolic Brain Disease | Ausgabe 3/2015

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Abstract

D-galactose (GAL) causes aging-related changes and oxidative stress in the organism. We investigated the effect of whole fresh blueberry (BB) (Vaccinium corymbosum L.) treatment on oxidative stress in age-related brain damage model. Rats received GAL (300 mg/kg; s.c.; 5 days per week) alone or together with 5 % (BB1) and 10 % (BB2) BB containing chow for two months. Malondialdehyde (MDA),protein carbonyl (PC) and glutathione (GSH) levels, and Cu Zn-superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities as well as acetylcholinesterase (AChE) activities were determined. Expressions of B cell lymphoma-2 (Bcl-2), Bax and caspase-3 were also evaluated in the brain by immunohistochemistry. MDA and PC levels and AChE activity increased, but GSH levels, SOD and GSH-Px activities decreased together with histopathological structural damage in the brain of GAL-treated rats. BB treatments, especially BB2 reduced MDA and PC levels and AChE activity and elevated GSH levels and GSH-Px activity. BB1 and BB2 treatments diminished apoptosis and ameliorated histopathological findings in the brain of GAL-treated rats. These results indicate that BB partially prevented the shift towards an imbalanced prooxidative status and apoptosis together with histopathological amelioration by acting as an antioxidant (radical scavenger) itself in GAL-treated rats.

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Titel: Blueberry treatment decreased D-galactose-induced oxidative stress and brain damage in rats
verfasst von: Jale Çoban
Işın Doğan-Ekici
A. Fatih Aydın
Esra Betül-Kalaz
Semra Doğru-Abbasoğlu
Müjdat Uysal
Publikationsdatum: 01.06.2015
Verlag: Springer US
Erschienen in: Metabolic Brain Disease / Ausgabe 3/2015
Print ISSN: 0885-7490
Elektronische ISSN: 1573-7365
DOI: https://doi.org/10.1007/s11011-014-9643-z

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