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Abstract Title:

Anti-oxidative effect of resveratrol on aluminum induced toxicity in rat cerebral tissue.

Abstract Source:

Bratisl Lek Listy. 2017 ;118(5):269-272. PMID: 28516788

Abstract Author(s):

M M H Zakaria, B Hajipour, R Estakhri, B M Saleh

Article Affiliation:

M M H Zakaria

Abstract:

INTRODUCTION: The direct protective effects of resveratrol against oxidative stress have been demonstrated in neuroglial cells, the mechanisms of these effects are not fully understood. The aim of this research was to study the effect of resveratrol on AL induced cerebral injury in rat.

METHODS: We divided the groups as follows with 10 animals each: a) Group I - served as control receiving normal drinking water and diet ad libitum. b) Group II - animals were administered aluminum at a dose level of 100 mg/kg body weight for a period of 6 weeks daily through oral gavage. c) Group III - animals were administered aluminum at a dose level of 100 mg/kg body weight and resveratrol at a dose of 10 mg/kg body weight intraperitoneally for a period of 6 weeks daily. After 6 weeks rats were anesthetized and decapitated. Brains were removed immediately and frozen in liquid nitrogenRESULTS: The levels of SOD and GPx antioxidant enzymes were decreased in all of the groups receiving aluminium, but it was less severe in resveratrol treated group. SOD and GPx levels in aluminium + resveratrol group were higher than in the aluminum group (p<0.05). MDA level, as an index of lipid peroxidation, increased significantly in all of the groups receiving aluminium. MDA level was lower in aluminium + resveratrol group compared to aluminum group and the difference was significant (p<0.05).

CONCLUSIONS: This study suggests that resveratrol is effective in preventing AL induced toxicity by reducing MDA production in cerebral tissue. Resveratrol also attenuated SOD and GPx suppression in cerebral tissue significantly. Our findings provide the rationale for further studies directed to understanding the mechanism of resveratrol in preventing neurodeterioration (Tab. 1, Ref. 35).

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