Journal of basic and clinical physiology and pharmacology · 2015
Geraniol attenuates oxidative stress by Nrf2 activation in diet-induced experimental atherosclerosis.
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Jayachandran Muthukumaran, Chandrasekaran Balaji, Namasivayam Nalini
Аннотация
BACKGROUND: Preclinical and clinical studies suggest the use of antioxidants as an effective measure to reduce the progression of oxidative-stress-related disorders. Nuclear factor E2-related factor 2 (Nrf2) is a key component to cellular redox homeostasis in the attenuation of oxidative-stress-associated pathological processes. The objective of the current study was to evaluate the role of geraniol (GOH) in preserving the plasma lipid status, endothelial function, antioxidant status, and inhibition of lipid peroxidation (LPO) in hamsters fed an atherogenic diet (AD).
METHODS: Male Syrian hamsters were randomly grouped into four groups: group 1 was control animals; group 2 was animals fed GOH alone (100 mg/kg bw po); group 3 was animals fed AD (standard pellet diet+10% coconut oil+0.25% cholesterol+0.25% cholic acid); and group 4 was fed AD+GOH (100 mg/kg bw) for 12 weeks. At the end of the feeding period, the animals were sacrificed and the liver, heart, and aorta from each group were analyzed for antioxidants, LPO markers, and histological changes.
RESULTS: AD feeding induced a significant change in lipid profile, endothelial function marker, activities of the antioxidant enzymes, alterations in the LPO markers, Nrf2 expression, and equally significant changes in the organ histology.
CONCLUSIONS: Supplementation with GOH appreciably prevented the alterations induced by the AD on all the above parameters. Thus, GOH offers marked protection against AD-induced abnormalities.
METHODS: Male Syrian hamsters were randomly grouped into four groups: group 1 was control animals; group 2 was animals fed GOH alone (100 mg/kg bw po); group 3 was animals fed AD (standard pellet diet+10% coconut oil+0.25% cholesterol+0.25% cholic acid); and group 4 was fed AD+GOH (100 mg/kg bw) for 12 weeks. At the end of the feeding period, the animals were sacrificed and the liver, heart, and aorta from each group were analyzed for antioxidants, LPO markers, and histological changes.
RESULTS: AD feeding induced a significant change in lipid profile, endothelial function marker, activities of the antioxidant enzymes, alterations in the LPO markers, Nrf2 expression, and equally significant changes in the organ histology.
CONCLUSIONS: Supplementation with GOH appreciably prevented the alterations induced by the AD on all the above parameters. Thus, GOH offers marked protection against AD-induced abnormalities.