PMID: 

Mol Med Rep. 2019 Jul 12. Epub 2019 Jul 12. PMID: 31322238

Abstract Title: 

The antidepressant effects of apigenin are associated with the promotion of autophagy via the mTOR/AMPK/ULK1 pathway.

Abstract: 

The present study aimed to investigate whether apigenin elicits antidepressant effects in depressant‑like mice via the regulation of autophagy. The depressant‑like behaviors were established in a chronic restraint stress model. Male BALB/c mice were subjected to restraint stress for 6 h/day for a period of 21 days, and deficits in sucrose preference, tail suspension and forced swim tests were confirmed to be improved following oral apigenin. To investigate the underlining mechanisms, the hippocampal levels of p62 and microtubule‑associated protein light chain 3‑II/I (LC3‑II/I) were measured using western blot analysis. The expression levels of LC3‑II/I and p62 indicated that the significantly inhibited autophagy level induced by chronic restraint stress can be increased following apigenin treatment. Similar to the level of autophagy, the expression levels of adenosine monophosphate‑activated protein kinase (AMPK) and Unc‑51 like autophagy activating kinase‑1 were downregulated after chronic restraint stress stimulation and, subsequently upregulated following treatment with apigenin. Conversely, the levels of mammalian target of rapamycin (mTOR) were increased in chronic restraint stress mice and inhibited by apigenin. Collectively, the present findings indicated that apigenin potentially promotes autophagy via the AMPK/mTOR pathway and induces antidepressive effects in chronic restraint stress mice.

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PMID: 

J Nutr Biochem. 2019 Jun 14 ;71:110-121. Epub 2019 Jun 14. PMID: 31325892

Abstract Title: 

Apigenin ameliorates HFD-induced NAFLD through regulation of the XO/NLRP3 pathways.

Abstract: 

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of liver-related morbidity and mortality disease in the world. However, no effective pharmacological treatment for NAFLD has been found. In this study, we used a high fat diet (HFD)-induced NAFLD model to investigate hepatoprotective effect of apigenin (API) against NAFLD and further explored its potential mechanism. Our results demonstrated that gavage administration of API could mitigate HFD-induced liver injury, enhance insulin sensitivity and markedly reduce lipid accumulation in HFD-fed mice livers. In addition, histological analysis showed that hepatic steatosis and macrophages recruitment in the API treatment group were recovered compared with mice fed with HFD alone. Importantly, API could reverse the HFD-induced activation of the NLRP3 inflammasome, further reduced inflammatory cytokines IL-1β and IL-18 release, accompanied with the inhibition of xanthine oxidase (XO) activity and the reduction of uric acid and reactive oxygen species (ROS) production. The pharmacological role of API was further confirmed using free fatty acid (FFA) induced cell NAFLD model. Taking together, our results demonstrated that API could protect against HFD-induced NAFLD by ameliorating hepatic lipid accumulation and inflammation. These protective effects may be partially attributed to the regulation of XO by API, which further modulated NLRP3 inflammasome activation and inflammatory cytokines IL-1β and IL-18 release. Therefore API is a potential therapeutic agent for the prevention of NAFLD.

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PMID: 

Artif Cells Nanomed Biotechnol. 2019 Dec ;47(1):2688-2697. PMID: 31257932

Abstract Title: 

Amygdalin reduces lipopolysaccharide-induced chronic liver injury in rats by down-regulating PI3K/AKT, JAK2/STAT3 and NF-κB signalling pathways.

Abstract: 

This study was aimed to evaluate the anti-inflammatory potential of AG on lipopolysaccharide (LPS) -induced liver injury and investigate the underlying mechanism. Administration of LPSs in the rat produced rat liver injury model which was ascertained at histological and molecular levels. Those models were treated with a range of doses of LPSs (0.5, 1.0 and 1.5 mg/kg body weight), followed by measurement physical parameter and function of the liver. Within the max treatment doses, no toxicity was shown but protective effects of AG were evidenced by regulation of physical parameters and functions of the liver. Interestingly, nuclear factor kappa B (NF-κB) levels and inflammatory factors were down-regulated by AG. Furthermore, the histopathological analysis demonstrated that AG promoted recovery from dysfunction of liver tissue in the rats, which was further confirmed by observing expression changes of inflammation-associated proteins. Particularly, alteration in the PI3K/AKT and JAK2/STAT3 signalling pathway protein expression were regulated by AG in a dose-dependent manner, indicating the mechanism underlying the relief effect of AG in liver injury. Our study demonstrated the potential of AG in the management of complications related to liver injury.

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PMID: 

Nutr Cancer. 2019 Jul 12:1-10. Epub 2019 Jul 12. PMID: 31298931

Abstract Title: 

Amygdalin Modulates Prostate Cancer Cell Adhesion and Migration In Vitro.

Abstract: 

The natural compound, amygdalin, is notably popular with prostate cancer patients as an alternative or complementary treatment option. However, knowledge about its mode of action is sparse. We investigated amygdalin's impact on prostate cancer adhesion and motile behavior. DU-145 and PC3 cancer cells were exposed to amygdalin. Adhesion to human vascular endothelium or immobilized collagen was then explored. The influence of amygdalin on chemotaxis and migration was also investigated, as well as amygdalin induced alteration to surface and total cellularα and β integrin expression. Integrin knockdown was performed to evaluate the integrin influence on chemotaxis and adhesion. Amygdalin significantly reduced chemotactic activity, migration, and adhesion of DU-145 but not of PC3 cells. Amygdalin elevated integrin α2 in both cell lines. Integrin α6 was reduced by amygdalin only in DU-145 cells, whereas β1 increased only in PC3 cells. Functional blocking revealed a negative association of α2 with PC3 and DU-145 chemotaxis. The β1 increase correlated with enhanced chemotaxis, the diminished α6 expression with reduced chemotaxis. Amygdalinacted on prostate cancer cells in vitro. It induced downregulation of α6 integrin in DU-145 but not in PC3 cells, suggesting that exposing certain prostate cancer cells to amygdalin might inhibit metastatic spread promoted by this particular integrin.

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PMID: 

Food Chem Toxicol. 2019 Jul 12 ;132:110674. Epub 2019 Jul 12. PMID: 31306687

Abstract Title: 

Aronia melanocarpa (Michx.) Elliot fruit juice reveals neuroprotective effect and improves cognitive and locomotor functions of aged rats.

Abstract: 

The aim of the study was to investigate the effect of polyphenol-rich Aronia melanocarpa (Michx.) Elliot juice (AMJ) on learning ability and memory, and brain morphology of aged rats. A model of healthy male Wistar rats (24 months of age) divided in 2 groups was used: AMJ group supplemented orally with AMJ (10 mL/kg for 105 days) and old control (CO) group without supplementation. Activity cage test showed that AMJ supplemented rats increased the number of vertical movements compared with old controls (p 

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PMID: 

Nutrients. 2019 Jun 29 ;11(7). Epub 2019 Jun 29. PMID: 31261928

Abstract Title: 

Mixed Nut Consumption May Improve Cardiovascular Disease Risk Factors in Overweight and Obese Adults.

Abstract: 

Emerging research indicates that nuts are a source of health-promoting compounds demonstrating cardioprotective benefits. However, most studies have assessed the effect of single nuts rather than a nut mixture. The objective of this study was, therefore, to examine the effect of mixed-nut consumption on cardiovascular disease (CVD) risk factors in overweight and obese adults. In a randomized, parallel-arm, controlled trial, 48 participants consumed isocaloric (250 kcal) amounts of pretzels or mixed-nuts. Body weight (BW) (= 0.024), BMI (= 0.043), and insulin levels (= 0.032) were significantly lower in the nut group compared to the pretzel group. Mixed-nut consumption also significantly reduced glucose (= 0.04) and insulin (= 0.032) levels after 4 and 8 weeks compared to baseline, respectively. Lactate dehydrogenase of the nut group was significantly lower than the pretzel group (= 0.002). No significant differences were detected between groups for triglycerides, LDL-C, and HDL-C. However, pretzel consumption increased triglycerides (= 0.048) from 4 weeks to 8 weeks. Moreover, LDL-C increased (= 0.038) while HDL-C transiently decreased (= 0.044) from baseline to 4 weeks. No significant lipid changes were detected within the nut group. Our results suggest that supplementing the diet with mixed-nuts could improve CVD risk factors by improving BW and glucose regulation in comparison to a common carbohydrate-rich snack without promoting the negative effects on lipids detected with pretzels.

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PMID: 

Nutrients. 2019 Jul 2 ;11(7). Epub 2019 Jul 2. PMID: 31269682

Abstract Title: 

Nut and Peanut Butter Consumption and Mortality in the National Institutes of Health-AARP Diet and Health Study.

Abstract: 

Although previous studies have shown inverse associations between nut consumption and mortality, the associations between nut consumption and less common causes of mortality have not been investigated. Additionally, about 50% of peanut consumption in the US is through peanut butter but the association between peanut butter consumption and mortality has not been thoroughly evaluated. The National Institutes of Health-AARP (NIH-AARP) Diet and Health Study recruited 566,398 individuals aged 50-71 at baseline in 1995-1996. A food-frequency questionnaire was used to evaluate nut and peanut butter consumption. Cox proportional hazard models were used to estimate hazard ratios and 95% confidence intervals for mortality using the non-consumers as reference groups and three categories of consumption. After excluding subjects with chronic diseases at baseline, there were 64,464 deaths with a median follow-up time of 15.5 years. We observed a significant inverse association between nut consumption and overall mortality (HR= 0.78, 95% CI = 0.76, 0.81,≤ 0.001). Nut consumption was significantly associated with reduced risk of cancer, cardiovascular, respiratory, infectious, renal and liver disease mortality but not with diabetes or Alzheimer's disease mortality. We observed no significant associations between peanut butter consumption and all-cause (HR= 1.00, 95% CI = 0.98, 1.04,= 0.001) and cause-specific mortality. In a middle-aged US population, nut intake was inversely associated with all-cause mortality and certain types of cause-specific mortality. However, peanut butter consumption was not associated with differential mortality.

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PMID: 

Nutrients. 2019 Jun 19 ;11(6). Epub 2019 Jun 19. PMID: 31248067

Abstract Title: 

Effect of Nut Consumption on Erectile and Sexual Function in Healthy Males: A Secondary Outcome Analysis of the FERTINUTS Randomized Controlled Trial.

Abstract: 

Lifestyle risk factors for erectile and sexual function include smoking, excessive alcohol consumption, lack of physical activity, psychological stress, and adherence to unhealthy diets. In the present study, we evaluated the effects of mixed nuts supplementation on erectile and sexual function. Eighty-three healthy male aged 18-35 with erectile function assessment were included in this FERTINUTS study sub-analysis; a 14-week randomized, controlled, parallel feeding trial. Participants were allocated to (1) the usual Western-style diet enriched with 60 g/day of a mixture of nuts (nut group;= 43), or (2) the usual Western-style diet avoiding nuts (control group;= 40). At baseline and the end of the intervention, participants answered 15 questions contained in the validated International Index of Erectile Function (IIEF), and peripheral levels of nitric oxide (NO) and E-selectin were measured, as surrogated markers of erectile endothelial function. Anthropometrical characteristics, and seminogram and blood biochemical parameters did not differ between intervention groups at baseline. Compared to the control group, a significant increase in the orgasmic function (-value = 0.037) and sexual desire (-value = 0.040) was observed during the nut intervention. No significant differences in changes between groups were shown in peripheral concentrations of NO and E-selectin. Including nuts in a regular diet significantly improved auto-reported orgasmic function and sexual desire.

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PMID: 

Eur J Pharmacol. 2019 Jul 5 ;859:172526. Epub 2019 Jul 5. PMID: 31283935

Abstract Title: 

Antidiabetic effects of pterostilbene through PI3K/Akt signal pathway in high fat diet and STZ-induced diabetic rats.

Abstract: 

Pterostilbene (PTE) is a natural dimethylated analog of resveratrol, which exerts antioxidative, hypolipidemic and hypoglycemic effects; however, the underlying mechanism is not yet clear. In this study, we evaluated the effects of PTE on diabetic rats and clarified the underlying mechanism. Diabetes was induced in rats by streptozotocin (STZ) and a high-sugar and high-fat diet. Rats were then treated with PTE (20, 40 and 80 mg/kg/d) for 8 weeks. Oral glucose tolerance test (OGTT) was performed to measure the glycometabolism of the diabetic rats at the end of the treatment. Fasting blood glucose (FBG), fasting insulin (FINS) and lipid profile were determined using an automatic biochemistry analyzer and serum inflammatory factors were analyzed by enzyme-linked immunosorbent assay. Serum superoxide dismutase (SOD) and malondialdehyde (MDA) were also analyzed by spectrophotometry to evaluate the anti-oxidant effects. The expression of proteins of PPARγ and PI3K/Akt signaling pathway related proteins in adipose tissue of the diabetic rats was analyzed by Western blotting. PTE treatment significantly reduced weight loss, FBG, insulin resistance, serum lipid levels and inflammatory factors. PTE treatment also inhibited oxidative stress by decreasing MDA expression and increasing SOD expression. Simultaneously,PTE treatment significantly ameliorated morphological impairment of the pancreas in diabetic rats. Furthermore, PTE treatment significantly increased the protein expression of PPARγ, PI3K, p-Akt, GLUT4 and IRS-1 in adipose tissues of diabetic rats. This study suggests that PTE can exert antidiabetic effects via the PI3K/Akt signaling pathway.

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PMID: 

Food Chem. 2019 Jun 17 ;299:125025. Epub 2019 Jun 17. PMID: 31295634

Abstract Title: 

Peanut protein-polyphenol aggregate complexation suppresses allergic sensitization to peanut by reducing peanut-specific IgE in C3H/HeJ mice.

Abstract: 

Peanut allergy is usually lifelong and accidental exposure impose formidable risk. The aim of this study was to assess the capacity of peanut proteins complexed to polyphenol extracts to reduce allergic response in C3H/HeJ mice. Mice were sensitized to peanut flour followed by exposure to amino acid diets fortified with peanut protein-polyphenol aggregates of either with low (15%; w/w) or high (40%; w/w) complexation ratios of blueberry (BB-Low and BB-High) and cranberry (CB-Low and CB-High) extracts. Treatment groups on diets with high complexation ratios of blueberry and cranberry aggregates showed significant reduction in peanut specific plasma Immunoglobulin E (IgE). Western blot analysis of spleen lysates showed CD63 protein expression was reduced in a dose-dependent manner in blueberry and cranberry complexed peanut protein supplemented diet groups. Our results demonstrate for the first time that complexation of polyphenols to peanut flour can potentially lower plasma IgE of peanut-sensitized C3H/HeJ mice.

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