Antioxidant and anti-inflammatory effects of flavocoxid in high-cholesterol-fed rabbits.

作者: Ahmed R El-Sheakh , Hamdy A Ghoneim , Ghada M Suddek , El-Sayed M Ammar , None

DOI: 10.1007/S00210-015-1168-4

关键词: FlavocoxidSuperoxide dismutaseHigh cholesterolAtorvastatinMalondialdehydeChemistryEndocrinologyImmunologyInternal medicineAntioxidantOxidative stressGlutathione

摘要: Flavocoxid is a mixed extract containing baicalin and catechin, it acts as dual balanced inhibitor of cyclooxygenase-1 (COX-1) COX-2 peroxidase enzyme activities with significant inhibition 5-lipoxygenase (5-LOX) activity in vitro. downregulates gene or protein expression several inflammatory markers exerts also strong antioxidant experimental models. Inflammation oxidative stress contribute the pathogenesis atherosclerosis. In present study, an rabbit model hypercholesterolemia was developed effects flavocoxid were evaluated. Rabbits divided into four groups-normal control, high-cholesterol-diet (HCD)-fed group, HCD plus (20 mg/kg/day), atorvastatin (10 mg/kg/day). Blood samples collected at end experiment for measuring serum total cholesterol (TC), triglycerides (TGs), high-density lipoprotein (HDL-C), C-reactive (CRP), malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD). addition, aorta removed measurement status, vascular reactivity, intima/media (I/M) ratio. Elevated levels TC, TGs, LDL-C, CRP measured group. Moreover, caused increase aortic MDA concomitantly reduction GSH SOD. Immunohistochemical staining specimens from HCD-fed rabbits revealed high both tumor necrosis factor-alpha (TNF-α) nuclear factor (NF)-κB. group showed significantly lower CRP, serum, higher HDL-C, SOD compared to HCD-induced elevations TC LDL-C did not affected by treatment. Additionally, enhanced endothelium-dependent relaxation acetylcholine decreased elevated I/M This effect confirmed histopathological examination aorta. effectively suppresses release markers. conclusion, these findings demonstrated that would be useful preventing stress, inflammation, dysfunction induced HCD.

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