Please use this identifier to cite or link to this item: http://hdl.handle.net/11189/6325
Title: Effects of kolaviron on hepatic oxidative stress in streptozotocin induced diabetes.
Authors: Oyenihi, OR 
Brooks, Nicole L 
Oguntibeju, OO 
Keywords: Diabetes;Antioxidant;Apoptosis;Liver
Issue Date: 2015
Publisher: BMC Complementary and Alternative Medicine
Journal: BMC Complementary and Alternative Medicine 
Abstract: Background: Alteration in antioxidant defence and increase in oxidative stress that results in tissue injury is characteristic of diabetes. We evaluated the protective effects of kolaviron (a flavonoid complex extracted from the seeds of Garcinia kola) on hepatic antioxidants, lipid peroxidation and apoptosis in diabetic rats. Methods: To induce diabetes, rats were injected with streptozotocin intraperitoneally at a single dose of 50 mg/kg. Kolaviron (100 mg/kg) was administered orally for 6 weeks (5 times weekly). Activities of liver antioxidant enzymes was analysed with Multiskan Spectrum plate reader. High performance liquid chromatography (HPLC) was used in the analysis of MDA (malondialdehyde), a product of lipid peroxidation. Apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Result: Diabetic rats exhibited a significant increase in the peroxidation of hepatic lipids as observed from the elevated level of malondialdehyde (MDA). In addition, Oxygen Radical Absorbance Capacity (ORAC), level of reduced glutathione (GSH), ratio of reduced to oxidized glutathione (GSH: GSSG) and catalase (CAT) activity were decreased in the liver of diabetic rats. The activities of GPX (glutathione peroxidase) and SOD (superoxide dismutase) were unaltered in diabetic rats. TUNEL assay revealed increased apoptotic cell death in the liver. Kolaviron attenuated lipid peroxidation and apoptosis, increased CAT activity, GSH levels and GSH: GSSG ratio. The ORAC of kolaviron-treated diabetic liver was restored to near-normal values. Conclusion: Kolaviron protects the liver against oxidative and apoptotic damage induced by hyperglycemia.
URI: http://hdl.handle.net/11189/6325
ISSN: 1472-6882
DOI: http://dx.doi.org/10.1186/s12906-015-0760-y
Appears in Collections:HWSci - Journal Articles (DHET subsidised)

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