Pomegranate juice ameliorates dopamine release and behavioral deficits in a rat model of parkinson’s disease

Pomegranate juice (PJ) is a rich source of ellagitannins (ETs), precursors of colonic metabolite urolithin A, which are believed to contribute to pomegranate’s neuroprotective effect. While many experimental studies involving PJ’s role in Alzheimer’s disease and hypoxic-ischemic brain injury have been conducted, our knowledge of pomegranate’s effects against Parkinson’s disease (PD) is very limited. Previously, we have reported that PJ treatment improved postural stability, which correlated well with enhancement of neuronal survival, protection against oxidative damage, and ?-synuclein aggregation. Since olfactory and motor deficits are typical symptoms of PD, in this study, we aimed to investigate the capability of PJ to protect against olfactory, motoric, and neuro-chemical alterations. To evaluate its efficiency, Wistar rats were given a combined treatment with ROT (1.3 mg/kg b.w./day, s.c.) and PJ (500 mg/kg/day, p.o.) for 35 days. After this, we assessed the olfactory discrimination index (DI) and vertical and horizontal activities as well as levels of dopamine and its main metabolite 3,4-Dihydroxyphenylacetic acid (DOPAC) in the dissected midbrain of animals. Our findings provide the first evidence that PJ treatment protects against ROT-induced DA depletion in the midbrain, which correlates well with improved olfactory function and vertical activity as well as with the presence of urolithin A in the brain

Influence of the Melissa officinalis

Melissa officinalis (MO, English: lemon balm, Lamiaceae), one of the oldest and still most popular aromatic medicinal plants, is used in phytomedicine for the prevention and treatment of nervous disturbances. The aim of our study was to assess the effect of subchronic (28-fold) administration of a 50% ethanol extract of MO leaves (200 mg/kg, p.o.) compared with rosmarinic acid (RA, 10 mg/kg, p.o.) and huperzine A (HU, 0.5 mg/kg, p.o.) on behavioral and cognitive responses in scopolamine-induced rats. The results were linked with acetylcholinesterase (AChE), butyrylcholinesterase (BuChE), and beta-secretase (BACE-1) mRNA levels and AChE and BuChE activities in the hippocampus and frontal cortex of rats. In our study, MO and HU, but not RA, showed an improvement in long-term memory. The results were in line with mRNA levels, since MO produced a decrease of AChE mRNA level by 52% in the cortex and caused a strong significant inhibition of BACE1 mRNA transcription (64% in the frontal cortex; 50% in the hippocampus). However, the extract produced only an insignificant inhibition of AChE activity in the frontal cortex. The mechanisms of MO action are probably more complicated, since its role as a modulator of beta-secretase activity should be taken into consideration

Polyphenols in Parkinson’s Disease: A Systematic Review of In Vivo Studies

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

What Is the Evidence that Parkinson’s Disease Is a Prion Disorder, Which Originates in the Gut?

Parkinson’s disease (PD) is a neurodegenerative disorder resulting from degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc). PD is characterized by motor dysfunctions as well as gastrointestinal symptoms and mental impairment. The pathological hallmark of PD is an accumulation of misfolded α-synuclein aggregates within the brain. The etiology of PD and related synucleinopathy is poorly understood, but recently, the hypothesis that α-synuclein pathology spreads in a prion-like fashion originating in the gut has gained much scientific attention. A crucial clue was the appearance of constipation before the onset of motor symptoms, gut dysbiosis and synucleinopathy in PD patients. Another line of evidence, demonstrating accumulation of α-synuclein within the peripheral autonomic nervous system (PANS), including the enteric nervous system (ENS), and the dorsal motor nucleus of the vagus (DMV) support the concept that α-synuclein can spread from the ENS to the brain by the vagus nerve. The decreased risk of PD following truncal vagotomy supports this. The convincing evidence of the prion-like behavior of α-synuclein came from postmortem observations that pathological α-synuclein inclusions appeared in healthy grafted neurons. In this review, we summarize the available data from human subjects’ research and animal experiments, which seem to be the most suggestive for explaining the hypotheses

Functional insights into recombinant TROSPA protein from Ixodes ricinus.

Lyme disease (also called borreliosis) is a prevalent chronic disease transmitted by ticks and caused by Borrelia burgdorferi s. l. spirochete. At least one tick protein, namely TROSPA from I. scapularis, commonly occurring in the USA, was shown to be required for colonization of the vector by bacteria. Located in the tick gut, TROSPA interacts with the spirochete outer surface protein A (OspA) and initiates the tick colonization. Ixodes ricinus is a primary vector involved in B. burgdorferi s. l. transmission in most European countries. In this study, we characterized the capacities of recombinant TROSPA protein from I. ricinus to interact with OspA from different Borrelia species and to induce an immune response in animals. We also showed that the N-terminal part of TROSPA (a putative transmembrane domain) is not involved in the interaction with OspA and that reduction of the total negative charge on the TROSPA protein impaired TROSPA-OspA binding. In general, the data presented in this paper indicate that recombinant TROSPA protein retains the capacity to form a complex with OspA and induces a significant level of IgG in orally immunized rats. Thus, I. ricinus TROSPA may be considered a good candidate component for an animal vaccine against Borrelia

Effects of Long-Term Dietary Administration of Kale (Brassica oleracea L. var. acephala DC) Leaves on the Antioxidant Status and Blood Biochemical Markers in Rats

Kale (Brassica oleracea L. var. acephala DC) is a leafy green vegetable which belongs to the Brassicaceae family, one of the most commonly cultivated and consumed edible plants. The aim of this study was to investigate the potential adverse effects and antioxidant properties of freeze-dried kale leaves in 90-day dietary experiment on Wistar rats. The kale leaf powder was added to a diet at levels: 10, 30, and 60 g/kg feed. The standard blood biochemical and hematological markers, antioxidant enzyme activities, level of lipid peroxidation, reduced glutathione content, and damage to DNA in the liver were measured. Antioxidant potential in serum was measured and expressed as Trolox equivalents antioxidant capacity (TEAC). The kale leaf phytochemicals, i.e., glucosinolates, phenolic acids and flavonols, were quantified. Major glucosinolates were glucoiberin (164.6 mg/100 g d.w.) and glucobrassicin (130.6 mg/100 g d.w.), whereas kaempferol (159.1 mg/100 g d.w.), quercetin (119.6 mg/100 g d.w.), and sinapic acid (73.8 mg/100 g d.w.) dominated among phenolics. The lowest dose of kale leaves augmented the activity of catalase by 34% in males and by 44% in females. The highest applied dose increased activities of glutathione reductase by 31%, superoxide dismutase by 27%, and glutathione S-transferase by 24% in males only. Kale administration did not affect the activities of glutathione peroxidase and paraoxonase 1, glutathione concentration, lipid peroxidation level, and the level of DNA damage in the liver and the whole blood leukocytes. TEAC increased upon all doses of kale leaves by 30–90% in males and by 40–90% in females. The diet with kale did not affect blood biochemical and hematological markers. Results confirm no adverse effects of dried kale leaves used in model rat’s diet up to 60 g/kg for 90 days. The changes in hepatic antioxidant enzymes and plasma TEAC suggest beneficial effect of kale leaves on the antioxidant status in rats. Interestingly, these changes were more pronounced in male versus female animals