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1- Department of Biology, Faculty of Basic Sciences, University of Shahid Chamran of Ahvaz, Ahvaz, Iran
2- Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran ;Department of pharmacology, Faculty of veterinary medicine, Shahid Chamran University of Ahvaz, Iran , h.najafzadeh.varrzi@gmail.com
3- Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran
2- Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran ;Department of pharmacology, Faculty of veterinary medicine, Shahid Chamran University of Ahvaz, Iran , h.najafzadeh.varrzi@gmail.com
3- Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran
Abstract: (140 Views)
Background: Exposure to neurotoxins increases the risk of neurodegenerative diseases. Oxidative stress and apoptosis play a central role in the initiation and progression of disorders. Estrogen decrease aggravates oxidative stress and apoptosis caused by neurodegenerative diseases in menopause woman. It is assumed, the use of resveratrol with its antioxidant and protective properties, which has common signaling pathways with estrogen, can be a useful therapeutic approach in preventing the development of oxidative stress and apoptosis.
Objective: The present study investigated the protective effect of resveratrol on the change of antioxidant and apoptotic factors caused by rotenone in the hippocampus of ovariectomized rats.
Methods: thirty female rats were divided into 5 groups of 6 including rotenone (5m/kg), ovariectomized (bilateral), ovariectomized + rotenone, ovariectomized + resveratrol(40m/kg), and ovariectomized + rotenone + resveratrol. Rotenone was administered intraperitoneally and resveratrol orally for 21 days. At the end, Malondialdehyde, superoxide dismutase (SOD) and expression of BAX and Bcl2 were measured in the hippocampus.
Results: Enzyme activity and Bcl2 expression in the rotenone and ovariectomized groups significantly were decreased. BAX expression and Malondialdehyde significantly were increased. Also Resveratrol significantly increased enzyme activity (57.9±1.94 U/mg protein) and Bcl2 expression (0.78±0.05) in ovariectomized + rotenone + resveratrol groups (P≤0.001). Also, resveratrol significantly reduced BAX expression (4.5±0.11) and Malondialdehyde (22.35±1.91 µM/g) in these groups (P≤0.001).
Conclusion: Resveratrol improved oxidative stress and apoptosis gene expression changes caused by rotenone and Absence of estrogen in the hippocampus.
Objective: The present study investigated the protective effect of resveratrol on the change of antioxidant and apoptotic factors caused by rotenone in the hippocampus of ovariectomized rats.
Methods: thirty female rats were divided into 5 groups of 6 including rotenone (5m/kg), ovariectomized (bilateral), ovariectomized + rotenone, ovariectomized + resveratrol(40m/kg), and ovariectomized + rotenone + resveratrol. Rotenone was administered intraperitoneally and resveratrol orally for 21 days. At the end, Malondialdehyde, superoxide dismutase (SOD) and expression of BAX and Bcl2 were measured in the hippocampus.
Results: Enzyme activity and Bcl2 expression in the rotenone and ovariectomized groups significantly were decreased. BAX expression and Malondialdehyde significantly were increased. Also Resveratrol significantly increased enzyme activity (57.9±1.94 U/mg protein) and Bcl2 expression (0.78±0.05) in ovariectomized + rotenone + resveratrol groups (P≤0.001). Also, resveratrol significantly reduced BAX expression (4.5±0.11) and Malondialdehyde (22.35±1.91 µM/g) in these groups (P≤0.001).
Conclusion: Resveratrol improved oxidative stress and apoptosis gene expression changes caused by rotenone and Absence of estrogen in the hippocampus.
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