PMID: 

Nutrients. 2019 Oct 3 ;11(10). Epub 2019 Oct 3. PMID: 31623329

Abstract Title: 

The Antimicrobial and Antiviral Activity of Polyphenols from Almond (L.) Skin.

Abstract: 

Due to their antimicrobial and antiviral activity potential in vitro, polyphenols are gaining a lot of attention from the pharmaceutical and healthcare industries. A novel antiviral and antimicrobial approach could be based on the use of polyphenols obtained from natural sources. Here, we tested the antibacterial and antiviral effect of a mix of polyphenols present in natural almond skin (NS MIX). The antimicrobial potential was evaluated against the standard American Type Culture Collection (ATCC) and clinical strains of, including methicillin-resistant (MRSA) strains, by minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC). Herpes simplex virus type I was used for the antiviral assessment of NS MIX by plaque assay. Furthermore, we evaluated the expression of viral cascade antigens. NS MIX exhibited antimicrobial (MIC values of 0.31-1.25 mg/ml) and antiviral activity (decrease in the viral titer **

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PMID: 

Nutrients. 2019 Feb 27 ;11(3). Epub 2019 Feb 27. PMID: 30818812

Abstract Title: 

In Vitro Digested Nut Oils Attenuate the Lipopolysaccharide-Induced Inflammatory Response in Macrophages.

Abstract: 

Nut consumption is known for its health benefits, in particular in inflammatory diseases. A possible mechanism for these effects could be their beneficial fatty acid composition. Nuts mainly contain mono- and polyunsaturated fatty acids, which have anti-inflammatory properties. However, studies investigating the effects of nut extracts on inflammatory processes on the molecular level are rare. We therefore prepared oily nut extracts after in vitro digestion and saponification of the fat-soluble constituents. Besides chromatographic analysis, cell culture experiments were performed using murine macrophages (RAW264.7) to study the capacity of different nut extracts (hazelnut, almond, walnut, macadamia, and pistachio) to modulate inflammatory processes. Oleic acid was the main fatty acid in hazelnut, almond, macadamia, and pistachio extracts. Both oily nut extracts and pure oleic acid significantly reduced the LPS-induced expression of iNos, Cox2, Tnfα, Il1β, and Il6 mRNAs. iNos protein expression was down-regulated followed by reduced nitric oxide formation. Thus, nut extracts at concentrations achievable in the digestive tract inhibit the expression and formation of inflammatory mediators in macrophages. Hence, a beneficial contribution of nut consumption to inflammatory diseases can be assumed. We are convinced that these results provide new insights on the molecular mechanisms involved in the health-beneficial effects of nuts.

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PMID: 

Food Chem. 2019 Oct 1 ;294:1-8. Epub 2019 Apr 25. PMID: 31126441

Abstract Title: 

Hazelnut consumption improves testicular antioxidant function and semen quality in young and old male rats.

Abstract: 

The effects of hazelnut supplemented diet on the reproductive system of young and old male rats were investigated. Young male rats were grouped into young control group (YCG) and young hazelnut group (YHG). Old male rats were grouped into old control group (OCG), old hazelnut group (OHG), and old vitamin E group (OEG). While YCG and OCG were given rat feed, YHG and OHG were given rat feed supplemented with hazelnut (3 g/kg body weight). OEG was subjected to rat feed and administered vitamin E (50 mg/kg body weight). When YCG and OCG were compared, aging increased histopathological damage and decreased sperm quality. Hazelnut supplemented diet improved histopathological variables, sperm quality, seminal plasma and plasma oxidative stress, seminal plasma vitamin E, and plasma testosterone levels in both groups. The present work suggests that hazelnut supplemented diet significantly improves testicular antioxidant function and semen quality in old male rats.

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PMID: 

Nutrients. 2019 Sep 14 ;11(9). Epub 2019 Sep 14. PMID: 31540081

Abstract Title: 

Dietary Supplementation with Hazelnut Oil Reduces Serum Hyperlipidemia and Ameliorates the Progression of Nonalcoholic Fatty Liver Disease in Hamsters Fed a High-Cholesterol Diet.

Abstract: 

: Hazelnut oil (HO) is rich in monounsaturated fatty acids and polyunsaturated fatty acids. This study intended to analyze the effects of hazelnut oil supplementation on the serum lipid profile and nonalcoholic fatty liver disease in hamsters fed a high-cholesterol (HC) diet.: Hamsters were fed a basic diet (control group) and an HC diet (HC group) for 16 weeks (= 10 in each group). Hamsters were fed an HC diet for four weeks to induce hyperlipidemia and were then fed an HC diet enriched with 5% (low-dose HC + HO group;= 10) and 10% HO (high-dose HC + HO group;= 10) for 12 weeks. Serum lipid levels, hepatic changes (including steatosis, inflammation, and fibrosis), and hepatic prooxidant-antioxidant status (malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione S-transferase (GST)) were evaluated after the treatment period.: Hamsters in the control group showed normal serum lipid profiles, normal liver function, and moderate glycogen storage without hepatic steatosis. Hamsters in the HC group showed severe hyperlipidemia, severe hepatic steatosis, and moderate steatohepatitis (mononuclear cell and neutrophil infiltration, oval cell hyperplasia, and fibrosis). Compared to the HC group, both the low-dose and the high-dose HC + HO groups showed a significant reduction of hyperlipidemia (serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and very-low-density lipoprotein cholesterol (VLDL-C levels)) and improved liver function (serum glutamic-oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT)). Additionally, compared to the HC group, intrahepatic triglyceride accumulation (IHTC) was significantly higher in the HC + HO group, while the incidence of steatohepatitis was significantly lower. The intake of the HC diet was associated with a higher level of lipid peroxidation (malondialdehyde, MDA) and a lower concentration of hepatic antioxidant enzymes (SOD, GPx, and GST), and all these factors were partially improved in the low-dose and high-dose HC + HO groups.Our findings indicate that the intake of HO reduced serum hyperlipidemia and oxidative stress and ameliorated the progression of nonalcoholic fatty liver disease in hamsters fed a high-cholesterol diet.

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PMID: 

Oxid Med Cell Longev. 2019 ;2019:4683723. Epub 2019 Jul 4. PMID: 31354906

Abstract Title: 

A Hazelnut-Enriched Diet Modulates Oxidative Stress and Inflammation Gene Expression without Weight Gain.

Abstract: 

Introduction: Inflammation is associated with obesity condition and plays a pivotal role in the onset and progression of many chronic diseases. Among several nutraceutical foods, hazelnuts (Corylus avellana L.) are considered an excellent anti-inflammatory and hypolipidemic food being the second richest source of monounsaturated fatty acids among nuts and because they are rich in vitamins, minerals, and phenolic compounds.Materials and Methods: A prospective pilot clinical trial on 24 healthy volunteers who consumed daily, as a snack, 40 g of hazelnuts (261.99 kcal/1096.17 kJ) for six weeks was conducted. Anthropometric measurements, body composition analysis, and nutrigenomic analysis on 12 anti-inflammatory and antioxidant genes were evaluated at baseline (T0) and after hazelnut intervention (T1).Results: No significant changes were detected on body composition analysis after hazelnut consumption. Conversely, significant upregulation was detected for SOD1 (2= 2.42), CAT (2= 2.41), MIF (2= 4.12), PPAR(2= 5.89), VDR (2= 3.61), MTHFR (2= 2.40), and ACE (2= 2.16) at the end of the study.Conclusions: According to emerging evidences, hazelnut consumption does not lead to weight gain probably due to the improvement of the body's antioxidant capacity by the upregulation of genes implied in oxidant reactions and inflammation.

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PMID: 

Nutr Rev. 2019 Oct 1 ;77(10):691-709. PMID: 31361320

Abstract Title: 

Nut consumption and incidence of cardiovascular diseases and cardiovascular disease mortality: a meta-analysis of prospective cohort studies.

Abstract: 

CONTEXT: Previous meta-analyses evaluating the association between nut consumption and the risk of cardiovascular disease (CVD) had substantial methodological limitations and lacked recently published large prospective studies; hence, making an updated meta-analysis highly desirable.OBJECTIVE: To update the clinical guidelines for nutrition therapy in relation to the European Association for the Study of Diabetes (EASD), a systematic review and meta-analysis of prospective studies was conducted using the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) system to summarize the evidence of the association between total nuts, specific types of nuts, and the incidence of, and mortality from, CVD outcomes.DATA SOURCES: Relevant articles were identified by searching the PubMed and Cochrane databases.DATA EXTRACTION: Two independent researchers screened the articles to identify those that met the inclusion criteria.DATA ANALYSIS: The inverse variance method with fixed-effect or random-effects models was used to pool data across studies (expressed as risk ratio [RR] and 95% confidence interval [CI]). Heterogeneity was tested and quantified using the Cochrane Q test and I2-statistic, respectively. The GRADE system was used to assess the quality of the evidence.RESULTS: Nineteen studies were included in the analyses. The results revealed an inverse association between total nut consumption (comparing highest vs lowest categories) and CVD incidence (RR, 0.85; 95%CI, 0.800.91; I2, 0%), CVD mortality (RR, 0.77; 95%CI, 0.72-0.82; I2, 3%), coronary heart disease (CHD) incidence (RR, 0.82; 95%CI, 0.69-0.96; I2, 74%), CHD mortality (RR, 0.76; 95%CI, 0.67-0.86; I2, 46%), stroke mortality (RR, 0.83; 95%CI, 0.75-0.93; I2, 0%), and atrial fibrillation (RR, 0.85; 95%CI, 0.73-0.99; I2, 0%). No association was observed with stroke incidence and heart failure. The certainty of the evidence ranged from moderate to very low.CONCLUSIONS: This systematic review and meta-analysis revealed a beneficial role of nut consumption in reducing the incidence of, and mortality from, different CVD outcomes.

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PMID: 

Antioxidants (Basel). 2019 Aug 12 ;8(8). Epub 2019 Aug 12. PMID: 31409026

Abstract Title: 

Health Benefits of Nut Consumption in Middle-Aged and Elderly Population.

Abstract: 

Aging is considered the major risk factor for most chronic disorders. Oxidative stress and chronic inflammation are two major contributors for cellular senescence, downregulation of stress response pathways with a decrease of protective cellular activity and accumulation of cellular damage, leading in time to age-related diseases. This review investigated the most recent clinical trials and cohort studies published in the last ten years, which presented the influence of tree nut and peanut antioxidant diets in preventing or delaying age-related diseases in middle-aged and elderly subjects (≥55 years old). Tree nut and peanut ingestion has the possibility to influence blood lipid count, biochemical and anthropometric parameters, endothelial function and inflammatory biomarkers, thereby positively affecting cardiometabolic morbidity and mortality, cancers, and cognitive disorders, mainly through the nuts' healthy lipid profile and antioxidant and anti-inflammatory mechanisms of actions. Clinical evidence and scientific findings demonstrate the importance of diets characterized by a high intake of nuts and emphasize their potential in preventing age-related diseases, validating the addition of tree nuts and peanuts in the diet of older adults. Therefore, increased consumption of bioactive antioxidant compounds from nuts clearly impacts many risk factors related to aging and can extend health span and lifespan.

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PMID: 

Life Sci. 2019 Oct 9 ;236:116948. Epub 2019 Oct 9. PMID: 31605711

Abstract Title: 

Ginsenoside Rg1 defenses PC-12 cells against hydrogen peroxide-caused damage via up-regulation of miR-216a-5p.

Abstract: 

BACKGROUND: Spinal cord injury (SCI) is a destructive trauma accompanied with local injury. Ginsenoside Rg1 exerts anti-apoptosis and anti-autophagy properties. Our goal was to study the protective mechanism of Rg1 in attenuating cell injury.METHODS: MiR-216a-5p inhibitor was transfected into PC-12 cells to verify the growth promoting roles of miR-216a-5p, then cells were pre-treated by Rg1 for 24 h and treated by 300 μM hydrogen peroxide (HO) for 1 h. Cell viability and apoptosis were tested through Cell Counting Kit-8 (CCK-8) and flow cytometry, respectively. Expression of miR-216a-5p and cell damage relative factors was tested via qRT-PCR and Western blot experiments.RESULTS: HOinduced cell activity suppression, apoptosis and clear autophagy well at the concentration of 300 μM Rg1 attenuated HO-induced cell injury at the concentration of 200 μM that it elevated cell activity, attenuated apoptosis and autophagy and activated phosphatidylinositol 3 kinase (PI3K)/AMP-activated protein kinase (AKT) and AMP-activated protein kinase (AMPK) signal pathways. Further, miR-216a-5p was up-regulated by Rg1.CONCLUSION: Our study demonstrated that Rg1 attenuated HO-caused cell injury through positively regulated miR-216a-5p.

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PMID: 

Med Sci Monit. 2019 Oct 3 ;25:7407-7417. Epub 2019 Oct 3. PMID: 31609302

Abstract Title: 

Ginsenoside Rb1 Prevents Dysfunction of Endothelial Cells by Suppressing Inflammatory Response and Apoptosis in the High-Fat Diet Plus Balloon Catheter-Injured Rabbit Model

Abstract: 

BACKGROUNDThe initiation of atherosclerosis (AS) is attributed to the dysfunction of endothelial cells (ECs) via the inhibition of g protein-coupled estrogen receptor (GPER). In the current study, we assessed the potential of Ginsenoside Rb1 (Rb1) to attenuate the dysfunction of ECs via GPER-mediated PI3K/Akt pathway.MATERIAL AND METHODSAS was induced in rabbits and then the AS rabbits were treated with Rb1. Thereafter, the ECs were isolated from AS and healthy rabbits, and treated with Rb1. The effect of Rb1 on blood lipid levels in AS rabbits and on apoptosis, inflammatory response, and GPER/PI3K/Akt axis activity in ECs was detected. Furthermore, the activities of GPER and PI3K were modulated to verify the key role of the axis in the anti-AS effect of Rb1.RESULTSThe levels of total cholesterol, low-density lipoprotein (LDL), and triglyceride in AS rabbits were suppressed by Rb1 while the high-density lipoprotein (HDL) level was increased. Inin vitroassays, Rb1 administration inhibited apoptosis process and the production of pro-inflammation cytokines in AS ECs. The expression levels of GPER, p-PI3K, and p-Akt were upregulated by Rb1, associated with the increased level of Bcl-2 and reduced level of Bax. When the activity of GPER was inhibited by GP-15 in AS ECs, the treatment effect of Rb1 was blocked. However, the activation of PI3K could restore the protective effect of Rb1 after the inhibition of GPER.CONCLUSIONSThe anti-AS potential of Rb1 was exerted by restoring the regular function of ECs via the activation of GPER-mediated PI3K/Akt signaling.

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PMID: 

Int J Mol Sci. 2019 Oct 5 ;20(19). Epub 2019 Oct 5. PMID: 31590397

Abstract Title: 

Ginsenoside Rb1 Attenuates High Glucose-Induced Oxidative Injury via the NAD-PARP-SIRT Axis in Rat Retinal Capillary Endothelial Cells.

Abstract: 

(1) Aims: The present study aimed to observe the effects of Ginsenoside Rb1 on high glucose-induced endothelial damage in rat retinal capillary endothelial cells (RCECs) and to investigate the underlying mechanism. (2) Methods: Cultured RCECs were treated with normal glucose (5.5 mM), high glucose (30 mM glucose), or high glucose plus Rb1 (20μM). Cell viability, lactate dehydrogenase (LDH) levels, the mitochondrial DNA copy number, and the intracellular ROS content were measured to evaluate the cytotoxicity. Superoxide dismutase (SOD), catalase (CAT), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX), poly(ADP-ribose) polymerase (PARP), and sirtuin (SIRT) activity was studied in cell extracts. Nicotinamide adenine dinucleotide (NAD)/NADH, NADPH/NADP, and glutathione (GSH)/GSSG levels were measured to evaluate the redox state. The expression of nicotinamide mononucleotide adenylyltransferase 1 (NMNAT1), SIRT1, and SIRT3 was also evaluated after Rb1 treatment. (3) Results: Treatment with Rb1 significantly increased the cell viability and mtDNA copy number, and inhibited ROS generation. Rb1 treatment increased the activity of SOD and CAT and reduced the activity of NOX and PARP. Moreover, Rb1 enhanced both SIRT activity and SIRT1/SIRT3 expression. Additionally, Rb1 was able to re-establish the cellular redox balance in RCECs. However, Rb1 showed no effect on NMNAT1 expression in RCECs exposed to high glucose. (4) Conclusion: Under high glucose conditions, decreases in the reducing power may be linked to DNA oxidative damage and apoptosis via activation of the NMNAT-NAD-PARP-SIRT axis. Rb1 provides an advantage during high glucose-induced cell damage by targeting the NAD-PARP-SIRT signaling pathway and modulating the redox state in RCECs.

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