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Background: Atherosclerosis is a major risk factor for the development of cardiovascular diseases. The aim of this study was to determine the effects of kambucha tea on oxidative stress induced by high cholesterol diet in New Zealand rabbits. Materials and Methods: In this experimental study, 32 New Zealand rabbits (weighing 2500-2000 g) were randomly divided into 4 groups of 8. The first group (control) received a standard diet and the second group (hypercholesterolemia) received a high cholesterol diet (1%) for 40 days. The third group received kambucha tea (gavage-day), and the fourth group received a high-cholesterol diet plus kambucha tea (10ml/kg). Eventually, serum levels of cholesterol, malondialdehyde, antioxidant capacity, and nitric oxide were determined. Results: Group receiving high cholesterol diet plus kambucha tea and group receiving only kambucha tea had significantly lower cholesterol level than the group receiving only high cholesterol diet (p < 0.0001, p = 0.03). Serum levels of MDA (malondialdehyde) in rabbits that received kambucha alone and kambucha plus high cholesterol diet were significantly lower compare with hypercholesterolemic groups (p = 0.001, p = 0.02). The group received the only kambucha, serum antioxidant capacity significantly increase compared to hypercholesterolemic group (p < 0.0001). Serum NO (nitric oxide) levels in rabbits that only received kambucha significantly decreased (p = 0.001). Conclusion: It can be argued that kambucha tea may be able to prevent the progression of atherosclerosis by improving the antioxidant defense system and preventing the oxidation of lipids.

The present study evaluates a hypothesis that diet-related hypercholesterolemia increases oxidative stress-related burden to cardiovascular tissue, resulting in progressively increased mortality, along with deterioration of electrophysiological and enzymatic function in rabbit myocardium. New Zealand white rabbits were divided into four groups, defined as follows: GROUP I, cholesterol-free rabbit chow for 12 weeks; GROUP II, cholesterol-free chow, 40 weeks; GROUP III, chow supplemented with 2% cholesterol, 12 weeks; GROUP IV, chow supplemented with 2% cholesterol, 40 weeks. At the 12 and 40 weeks time points, animals in each of the aforementioned cohorts were subjected to echocardiographic measurements, followed by sacrifice. Significant deterioration in major outcome variables measured in the present study were observed only in animals maintained for 40 weeks on 2% cholesterol-supplemented chow, with much lesser adverse effects noted in animals fed high cholesterol diets for only 12 weeks. It was observed that rabbits receiving high cholesterol diets for 40 weeks exhibited significantly increased mortality, worsened ejection fraction and general deterioration of cardiac functions, along with increased atherosclerotic plaque formation and infarct size. Additionally, myocardium of GROUP IV animals was observed to contain lower levels of heme oxygenase-1 (HO-1) and cytochrome c oxidase III (COX III) protein relative to the controls.

The present study evaluates a hypothesis that diet-related hypercholesterolemia increases oxidative stress-related burden to cardiovascular tissue, resulting in progressively increased mortality, along with deterioration of electrophysiological and enzymatic function in rabbit myocardium. New Zealand white rabbits were divided into four groups, defined as follows: GROUP I, cholesterol-free rabbit chow for 12 weeks; GROUP II, cholesterol-free chow, 40 weeks; GROUP III, chow supplemented with 2% cholesterol, 12 weeks; GROUP IV, chow supplemented with 2% cholesterol, 40 weeks. At the 12 and 40 weeks time points, animals in each of the aforementioned cohorts were subjected to echocardiographic measurements, followed by sacrifice. Significant deterioration in major outcome variables measured in the present study were observed only in animals maintained for 40 weeks on 2% cholesterol-supplemented chow, with much lesser adverse effects noted in animals fed high cholesterol diets for only 12 weeks. It was observed that rabbits receiving high cholesterol diets for 40 weeks exhibited significantly increased mortality, worsened ejection fraction and general deterioration of cardiac functions, along with increased atherosclerotic plaque formation and infarct size. Additionally, myocardium of GROUP IV animals was observed to contain lower levels of heme oxygenase-1 (HO-1) and cytochrome c oxidase III (COX III) protein relative to the controls. [ABSTRACT FROM AUTHOR]

This Special Issue of the Journal of Alzheimer's Disease (JAD) provides an overview of animal models of Alzheimer's disease (AD). Very few species spontaneously develop the cognitive, behavioral, and neuropathological symptoms of AD, yet AD research must progress at a more rapid pace than the rate of human aging. In recent years, a variety of models have been created – from tiny invertebrates with life spans measurable in months to huge mammals that live several decades. The fruit fly, Drosophila melanogaster, is a powerful genetic tool that has recently emerged as a model of AD with neural features and assessable learning and memory. Transgenic mice are the most widely used animal models of AD and have yielded significant research breakthroughs. Accelerated aging seen in the SAMP8 mouse is a non-transgenic model with great utility. Rat models provided early evidence about the deleterious impact of amyloid-β (Aβ) on neurons and continue to provide insights. Rabbits, as langomorphs, are more closely related to primates than are rodents and have conserved the sequence of Aβ in humans (as have canines and non-human primates). The hypercholesterolemic rabbit is an excellent AD model. The aging canine develops AD neuropathology spontaneously and is especially suitable for tests of therapeutics. Non-human primates are invaluable for the development of therapeutics translating to humans. Each animal model has limitations and strengths, but used together in complementary fashion, animal models for research on AD are essential for rapid progress toward a cure. [ABSTRACT FROM AUTHOR]