No abstract

Pomegranate juice is a rich source of ellagitannins (ETs) believed to contribute to a wide range of pomegranate’s health benefits. While a lot of experimental studies have been devoted to Alzheimer disease and hypoxic-ischemic brain injury, our knowledge of pomegranate’s effects against Parkinson’s disease (PD) is very limited. It is suggested that its neuroprotective effects are mediated by ETs-derived metabolites—urolithins. In this study, we examined the capability of pomegranate juice for protection against PD in a rat model of parkinsonism induced by rotenone. To evaluate its efficiency, assessment of postural instability, visualization of neurodegeneration, determination of oxidative damage to lipids and α-synuclein level, as well as markers of antioxidant defense status, inflammation, and apoptosis, were performed in the midbrain. We also check the presence of plausible active pomegranate ETs-derived metabolite, urolithin A, in the plasma and brain. Our results indicated that pomegranate juice treatment provided neuroprotection as evidenced by the postural stability improvement, enhancement of neuronal survival, its protection against oxidative damage and α-synuclein aggregation, the increase in mitochondrial aldehyde dehydrogenase activity, and maintenance of antiapoptotic Bcl-xL protein at the control level. In addition, we have provided evidence for the distribution of urolithin A to the brain.

No abstract

Parkinson’s disease (PD) is the second most common neurodegenerative disorder. However, therapeutic options treating only its symptoms are very disappointing. Therefore there is an ongoing search for compounds capable of tackling the multi-dimensional features of PD. Recently natural polyphenols have gained great interest as potential therapeutic agents. Herein, we have attempted to summarize results obtained in different animal models demonstrating their neuroprotective effects. The in vivo findings presented below are supported by human subject data and reports regarding the ability of polyphenols to cross the blood-brain barrier. The beneficial effects of polyphenols are demonstrated by the results of behavioral examinations, mainly related to motor and cognitive capabilities, histopathological and immunohistochemical examination concerning the protection of dopaminergic neurons, analyses of dopamine and the concentration of its metabolites, as well as mechanistic studies regarding the modulation of oxidative stress, neuroinflammation, cellular iron management, proteinopathy, and additionally the regulation of signaling pathways. Importantly, data about brain distribution of the metabolic derivatives of the reviewed polyphenols are crucial for the justification of their nutritional intake in neuroprotective intervention, as well as for the identification of potential targets for a novel therapeutic approach to Parkinson’s disease.

The aim of the study was to investigate the potential protective effect of beetroot juice in a model of oxidative stress induced by N-nitrosodiethylamine (NDEA) and carbon tetrachloride (CCl(4)). Male Wistar rats were treated with beetroot juice per os, 8 mL/kg/day for 28 days, and a single i.p. dose of the xenobiotics: 150 mg/kg NDEA or 2 mL/kg CCl(4). Simultaneously, two groups of rats not pretreated with juice were given only each of the xenobiotics. The level of microsomal lipid peroxidation in the liver, expressed as TBARS concentration, was increased several fold in rats administered only NDEA or CCl(4). TBARS were decreased by 38% only in rats pretreated with beetroot juice before the administration of CCl(4). In animals pretreated with juice and receiving NDEA, a further increase in TBARS occurred. All of the investigated antioxidant enzymes were inhibited by the administration of either toxicant alone by 26%-77% as compared to controls. Pretreatment with juice caused a partial recovery in the activity of glutathione peroxidase and glutathione reductase, by 35% and 66%, respectively. Superoxide dismutase activity was increased about 3-fold in animals pretreated with juice. Both xenobiotics caused a rise in plasma protein carbonyls, which were reduced by 30% in rats pretreated with juice and then injected with NDEA. Similarly, DNA damage in blood leukocytes caused by either toxicant was slightly diminished, by 20%, in the rats treated with juice before NDEA administration. It could be concluded that pretreatment with beetroot juice can counteract, to some extent, xenobiotic-induced oxidative stress in rats.