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.
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.
Authors: Farida Larit; Khaled M Elokely; Narayan D Chaurasiya; Samira Benyahia; Manal A Nael; Francisco León; Mohammad Sanad Abu-Darwish; Thomas Efferth; Yan-Hong Wang; Djamila Belouahem-Abed; Samir Benayache; Babu L Tekwani; Stephen J Cutler Journal: Phytomedicine Date: 2017-12-27 Impact factor: 5.340
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