Maillard Reaction Products and Phenolic Compounds from Roasted Peanut Flour Extracts Prevent Scopolamine-Induced Amnesia Via Cholinergic Modulation and Antioxidative Effects in Mice.

Research on the beneficial effects of Maillard reaction products (MRPs) and phenolic compounds derived from roasted peanut flour on the nervous system remains insufficient. This study aimed to evaluate the effect of a 28-day oral administration of defatted peanut extract rich in MPRs and polyphenolic compounds on the cognitive impairments and oxidative injury induced by scopolamine in a mouse model. Light and dark extracts from peanut flour were prepared by heating peanuts at 187°C for two different times (8.6 and 12.7 min) and defatted using soxhlet apparatus. The mice were orally pretreated with either roasted defatted peanuts extracts (100 mg/kg) or donepezil (3 mg/kg) for 21 days. On day 19 and until day 28, mice were injected subcutaneously with water or scopolamine (1 mg/kg body weight) 15 min after roasted defatted peanuts extracts/water feeding. Mice were subsequently subjected to a battery of behavioral tests including open field locomotor activity assay, and Morris water maze test. Brain tissues were collected to measure acetylcholine, acetylcholinesterase, and oxidative parameters (glutathione and malondialdehyde). Roasted defatted peanuts (light and dark) (100 mg/kg) treatment significantly ameliorated cognitive performance and reversed the oxidative damage when compared with the scopolamine group. These data demonstrate the defatted peanuts extracts exert potent anti-amnesic effects via the modulation of cholinergic and antioxidant activities.

7ß-hydroxycholesterol-induced cell death, oxidative stress, and fatty acid metabolism dysfunctions attenuated with sea urchin egg oil.

Some oxysterols resulting either from enzymatic oxidation or autoxidation of cholesterol are associated with age-related diseases including neurodegenerative diseases. Among these oxysterols, 7ß-hydroxycholesterol (7ß-OHC) is often found at increased levels in patients. It is therefore important to identify molecules or mixtures of molecules to prevent 7ß-OHC-induced side effects. Consequently, murine oligodendrocytes (158N) were cultured in the absence or presence of 7ß-OHC (20 µg/mL, 24 h) with or without a natural oil extracted from sea urchin (Paracentrotus lividus) eggs known for its biological activity. Firstly, the chemical composition of this oil was determined using 31P NMR and GC-MS. Secondly, this oil was used to reduce 7ß-OHC-induced side effects. To this end, the oil (160 µg/mL) was added to the culture medium of 158N cells 2 h before 7ß-OHC. The effects of 7ß-OHC with or without the oil on cell viability were studied with the MTT test. Photometric methods were used to analyze antioxidant enzyme activities, superoxide dismutase (SOD) and glutathione peroxidase (GPx), as well as the generation of lipid peroxidation products (malondialdehyde (MDA), conjugated dienes (CDs)) and protein oxidation product (carbonylated proteins (CPs)). Gas chromatography was used to determine the fatty acid profile. With 7ß-OHC, an induction of cell death associated with oxidative stress (alteration of GPx and SOD activities) was observed; an overproduction of lipid peroxidation products (MDA and CDs) and CPs was also revealed. Sea urchin egg oil attenuated 7ß-OHC-induced cytotoxicity: 7ß-OHC-induced cell death was reduced, GPx and SOD activities were normalized, and lower levels of MDA, CDs and CPs were produced. In addition, whereas a disturbed fatty acid profile was observed with 7ß-OHC, similar fatty acid profiles were found in control cells and in cells cultured with 7ß-OHC associated with sea urchin egg oil. These data demonstrate the protective activities of sea urchin egg oil against 7ß-OHC-induced side effects on 158N cells, supporting the concept that this oil may have benefits in the prevention of neurodegenerative diseases.

Inhibition of protein glycation, antioxidant and antiproliferative activities of Carpobrotus edulis extracts.

Carpobrotus edulis is an important South African medicinal plants used as a food and therapeutic agent in traditional medicine. The aim of this study was to determine the phytochemical content, antioxidant, antiglycation and cytotoxic effect against Human Colon Cancer Cell Line (HCT-116) of aqueous and ethanol-water (1:1v/v) extracts of Carpobrotus edulis.The content of total phenolics and flavonoids in aqueous and ethanol-water extract were 151.99µg and 66.35µg gallic acid equivalents/mg of dry extract, and 38.84µg and 21.96µg quercetin/mg of dry extract, respectively. Furthermore, phenolic compositions analysis indicated the presence of seven majority compounds including sinapic acid, ferulic acid, luteolin7-o-glucoside, hyperoside, isoquercitrin, ellagic acid and isorhamnetin 3-O-rutinoside. The ethanol-water extract (100-1000µg/mL) showed better antioxidant activity than aqueous extract. Furthermore, Carpobrotus edulis extracts, especially ethanol-water extract significantly inhibited the formation of fluorescent advanced glycation end products, prevented oxidation-induced protein damage and exhibited a cytotoxic effect against HCT116 cells, with a significant decrease in cell viability after 24h of incubation. The results obtained suggest that the Carpobrotus edulis extracts could be used as an easily accessible source of natural antioxidants and as potential phytochemicals against protein glycation and colon cancer.

Analysis of association between bleomycin hydrolase and apolipoprotein E polymorphism in Alzheimer's disease.

Alzheimer's disease (AD) is the leading cause of dementia. Several studies indicate a possible relationship between different genes and Alzheimer's disease. To further investigate, we have analyzed the association between the bleomycin hydrolase (BLMH) and apolipoprotein E (ApoE) polymorphisms in 93 AD patients and age- and sex-matched 113 controls from the Tunisian population. The frequency of ApoE epsilon 4 allele was found to differ significantly in AD patients compared to the control [29.5% vs. 8.8 (χ (2) = 26, df = 1, p < 0.001)] leading to an increased risk of AD in subjects with this allele (OR = 3.29, 95% CI = 1.7-6.5; p = 0.001]. This risk was found to decrease from OR = 8.4, CI = 3.3-23; p < 0.001 in subjects less than 75 years old to OR = 1.2, CI = 1.031-14; p = 0.0297 in subjects 75 years and older. No association was observed between carrying the BLMH-G genotype and AD in ε4 negative or positive subjects.

-1154G/A and -2578C/A polymorphisms of the vascular endothelial growth factor gene in Tunisian Alzheimer patients in relation to beta-amyloid (1-42) and total tau protein.

Recent evidences indicate that polymorphisms within the promoter region of the vascular endothelial growth factor (VEGF) gene may elevate the risk for Alzheimer's disease (AD). To further investigate, we have analyzed association between promoter polymorphisms of the VEGF gene in 93 AD patients and age and sex matched 113 controls from Tunisian population. The distribution of genotype and allele frequencies of the VEGF (-2578C/A) and (-1154G/A) polymorphisms did not differ significantly between AD and control groups (p>0.05). In the subgroup of ApoE varepsilon4 carriers, the -2578A was observed to be significantly higher in the AD patients than in the control individuals. After adjusting the data by gender, age and the ApoE varepsilon4 status using logistic regression, the -2578A allele was found to increase the risk for sporadic AD by 1.7-fold. The present study provides the evidence that the -2578A allele may be associated with the development of AD in the individuals with ApoE varepsilon4 allele. In addition, AD patients carrying the -2578A allele had lower Abeta42 (p=0.029) levels than those without this allele, particularly in subjects with ApoE varepsilon4 allele.