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Protective role of chrysin against oxidative stress in d ‐galactose‐induced aging in an experimental rat model
Author(s) -
Anand Kalaiselvi Velayutham,
Mohamed Jaabir Mohamed Sultan,
Thomas Philip A,
Geraldine Pitchairaj
Publication year - 2012
Publication title -
geriatrics and gerontology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 57
eISSN - 1447-0594
pISSN - 1444-1586
DOI - 10.1111/j.1447-0594.2012.00843.x
Subject(s) - chrysin , malondialdehyde , oxidative stress , glutathione peroxidase , superoxide dismutase , endocrinology , glutathione , glutathione reductase , vitamin c , medicine , antioxidant , catalase , pharmacology , chemistry , biochemistry , enzyme , flavonoid
Aim:  To evaluate the putative protective role of chrysin, an isoflavone, on d ‐galactose‐induced aging in an experimental rat model. Methods:  Rats were divided into five groups of five each. Group I received 0.9% saline only. Groups II, III and IV received d ‐galactose (50 mg/kg bodyweight) intraperitoneally, additionally group III and group IV received chrysin (20 mg/kg bodyweight) and α‐tocopherol acetate (200 mg/kg bodyweight), respectively. Group V received chrysin alone. The experiment period was for a period of 8 weeks. After the rats were killed, the tissue samples were analyzed for mean activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione‐S‐transferase, glutathione reductase, glucose‐6‐phosphate dehydrogenase, reduced glutathione, vitamin C, vitamin E, malondialdehyde and protein carbonyl. Histopathological studies were also carried out for morphological conformation. Results:  Tissue samples from d ‐galactose‐exposed untreated rats showed significantly ( P  < 0.05) lower levels of enzymatic and non‐enzymatic anti‐oxidants, and significantly ( P  < 0.05) higher levels of malondialdehyde and protein carbonyl when compared with group I and group III rats. Oral administration of chrysin for a period of 8 weeks, concomitant with the exposure to d ‐galactose, appeared to protect against oxidative damage and maintained all parameters at near normal levels. Histopathological studies confirmed the oxidative damage caused by d ‐galactose alone in tissues and also showed the tissue protective role of chrysin in rats receiving d ‐galactose and chrysin. Conclusion:  These results suggest that chrysin protects against oxidative stress‐induced tissue damage in d ‐galactose‐induced aging in an experimental rat model. Geriatr Gerontol Int 2012; ••: ••–••.

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