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.

The aim of this study was to compare the protective effects of chokeberry juice and silymarin against chemical-induced liver fibrosis in rats. Liver fibrosis was induced by CCl4 administered two days a week for six weeks. Two groups of rats were co-treated with chokeberry juice, 10 mL/kg/day. or silymarin as a positive control, 100 mg/kg/day for six weeks. Hepatic lipid peroxidation was suppressed by 50% and the activity of hepatic antioxidant enzymes was increased by 19%–173% in rats co-treated with CCl4 and substances tested as compared to rats administered CCl4 alone. Hepatic hydroxyproline was decreased by 24% only in rats treated with silymarin. The messenger RNA (mRNA) expression levels of fibrosis-related molecules, procollagen I, α-SMA, TIMP-1, TGFβ, and TNFα, which were significantly increased in the liver of CCl4-treated rats, were not modulated by substances tested. Histological evaluation revealed a slight protective effect of silymarin against fibrosis. However, in CCl4 + chokeberry-treated rats, the density of vacuolated hepatocytes was significantly lower than that in silymarin administered animals. Chokeberry juice did not demonstrate an antifibrotic effect in the applied experimental model of fibrosis, and the effect of the known antifibrotic agent, silymarin, was very limited.

The high polyphenols content of cranberry accounts for its strong antioxidant activity underlying the beneficial health effects of this fruit. Rotenone (ROT) is a specific inhibitor of mitochondrial complex I in the brain which leads to the generation of oxidative stress. To date, there are few data indicating that toxicity of ROT is not limited to the brain but can also affect other tissues. We aimed to examine whether ROT-induced oxidative stress could be counteracted by cranberry juice not only in the brain but also in the liver and kidney. Wistar rats were given the combined treatment with ROT and cranberry juice (CJ) for 35 days. Parameters of antioxidant status were determined in the organs. ROT enhanced lipid peroxidation solely in the brain. The increase in the DNA damage was noticed in all organs examined and in leukocytes. The beneficial effect of CJ on these parameters appeared only in the brain. Additionally, CJ decreased the activity of serum hepatic enzymes. The effect of CJ on antioxidant enzymes was not consistent, however, in some organs, CJ reversed changes evoked by ROT. Summing up, ROT can cause oxidative damage not only in the brain but also in other organs. CJ demonstrated a protective effect against ROT-induced toxicity.

Abstract. Background Since primary liver cancer is the third leading cause of cancer mortality worldwide, chemopreventive strategies aimed at reducing its risk or delaying its onset are highly desirable. The most common type of primary liver cancer is an inflammation-associated cancer developing from hepatocytes, hepatocellular carcinoma (HCC). Hepatocarcinogenesis progresses from chronic intrahepatic inflammation within the state of oxidative stress, which results in continuous cellular injury, necrosis and regeneration along with a genotoxic effect (1, 2). Despite a clear viral etiology, HCC is also mediated through exposure to hepatocarcinogens such as nitrosamines, which cause the generation of radicals or cellular mitochondrial dysfunction (2).White mulberry (Morus alba) leaves contain abundant varieties of polyphenols, including chlorogenic acid, rutin, isoquercitrin, quercetin, astragalin and kaempferol, which are considered strong antioxidants (3). Mulberry leaf extract has been reported to scavenge 1,1-diphenyl-2-picryl-hydrazyl radical and prevent lipid peroxidation in rabbit and human low-density lipoproteins (4). Its antioxidant effect has been also revealed in streptozotocin-induced diabetic rats (5). Anticancer properties of mulberry leaf polyphenols have been demonstrated in numerous assays with various types of human cancer cells of colon (6), liver (7), breast (6), and lung (8), and the underlying mechanisms including antioxidant, antiinflammatory, and proliferative, and cytotoxic activity have been shown. However, to the best of our knowledge, the anticancer effect in an animal model has not yet been investigated.The present study was designed to evaluate the chemopreventive effect of mulberry leaf extract on Nnitrosodiethylamine (NDEA)-induced liver carcinogenesis in rats. This experimental model of hepatocarcinogenesis, due to histological and biochemical similarities between rodents and human hepatic lesions, is widely used in chemoprevention studies (9). Materials and MethodsMaterials. Dried and crushed M. alba L. (var. wielkolistna zolwinska) leaves were mixed with water (80-90˚C) using a counterflow process (1:10 w/w) and subjected to continuous extraction in a twin-screw extractor (IBPRS, Poznan, Poland). The resulting extract was then concentrated using a vacuum periodic spherical evaporator

Rich in polyphenols, cranberry juice (CJ) with high antioxidant activity is believed to contribute to various health benefits. However, our knowledge of the neuroprotective potential of cranberries is limited. Previously, we have demonstrated that CJ treatment controls oxidative stress in several organs, with the most evident effect in the brain. In this study, we examined the capability of CJ for protection against Parkinson’s disease (PD) in a rotenone (ROT) rat model. Wistar rats were administered with CJ in a dose of 500 mg/kg b.w./day (i.g.) and subcutaneously injected with ROT (1.3 mg/kg b.w./day). The experiment lasted 45 days, including 10 days pre-treatment with CJ and 35 days combined treatment with CJ and ROT. We quantified the expression of α-synuclein and apoptosis markers in the midbrain, performed microscopic examination, and assessed postural instability to evaluate the CJ neuroprotective effect. Our results indicate that the juice treatment provided neuroprotection, as evidenced by declined α-synuclein accumulation, Bax and cleaved/active caspase-9 expression, and normalized cytochrome c level that was accompanied by the enhancement of neuronal activity survival and improved postural instability. Importantly, we also found that long-term administration of CJ alone in a relatively high dose may exert a deleterious effect on cell survival in the midbrain.