PMID: 

J Cardiovasc Pharmacol. 2019 Sep 14. Epub 2019 Sep 14. PMID: 31599782

Abstract Title: 

Ginsenoside Re preserves cardiac function and ameliorates left ventricular remodeling in a rat model of myocardial infarction.

Abstract: 

Ginsenoside Re, an herbal ingredient from ginseng, has been demonstrated to protect the heart from various cardiovascular diseases. In the present study, we investigated the protective effects and mechanisms of ginsenoside Re (Gin-Re) on cardiac function and left ventricular remodeling in a rat model of myocardial infarction (MI). After ligating the left anterior descending coronary artery, Wistar rats were treated with Gin-Re (135 mg/kg) by gavage everyday for 4 weeks. Serological detection showed that Gin-Re significantly inhibited myocardial injury and attenuated oxidative stress in MI rats. Echocardiographic observation showed that Gin-Re significantly improved cardiac function and prevented left ventricular dilatation induced by MI. Pathological observation found that Gin-Re significantly decreased interstitial fibrosis in the left ventricle of MI rats. Compared with the MI group, Gin-Re treatment promoted AMPKα phosphorylation, decreased TGF-β1 expression and attenuated Smad2/3 activation. After Gin-Re treatment, the phosphorylation of FAK, PI3K p110α and Akt was enhanced in MI rats, while PI3K p110β showed no difference compared with the MI group. These results indicate that Gin-Re may improve MI-induced cardiac dysfunction and mitigate ventricular remodeling via regulation of the AMPK/TGF-β1/Smad2/3 and FAK/PI3K p110α/Akt signaling pathways.

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PMID: 

EXCLI J. 2019 ;18:666-676. Epub 2019 Aug 22. PMID: 31611749

Abstract Title: 

Cytoprotective effects of ginsenoside Rd on apoptosis-associated cell death in the isolated human pancreatic islets.

Abstract: 

Ginsenoside Rd (GS-Rd), one of the main pharmacologically active components of ginseng, has shown the potential to stabilize mitochondrial membrane integrity and decrease apoptotic death in neuronal and non-neuronal cells. The present study aimed to evaluate the effect of this bioactive molecule on the apoptosis-associated cell death in human pancreatic islets. In this regard human pancreatic islets were isolated and grouped for the treatment with GS-Rd. The isolated islets were treated with different concentrations of GS-Rd. After 24 and 72 h of incubation, the islets were evaluated in terms of viability,,, and insulin gene expression, BAX, BCL2, and caspase-3 protein expression, apoptosis, and glucose-induced insulin/C-peptide secretion. Our results revealed the islet survival was significantly decreased in the control group after 72 h of incubation. However, GS-Rd inhibited the progress of the islet death in the treated groups. TUNEL staining revealed that the preventive effect of this molecule was caused by the inhibition of apoptosis-associated death. In this regard, the activation of caspase-3 was down-regulated in the presence of GS-Rd. GS-Rd did not exhibit undesirable effects on glucose-induced insulin and C-peptide stimulation secretion. In conclusion, GS-Rd inhibited the progress of death of cultured human pancreatic islets by diminishing the apoptosis of the islet cells.

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PMID: 

Biomed Pharmacother. 2019 Oct 16 ;120:109483. Epub 2019 Oct 16. PMID: 31629252

Abstract Title: 

Ginsenoside Rg3 regulates DNA damage in non-small cell lung cancer cells by activating VRK1/P53BP1 pathway.

Abstract: 

Lung cancer is the leading cause of cancer-related deaths. Ginsenoside Rg3 is the main ingredient of Ginseng which is used to treat non-small cell lung cancer (NSCLC). It has been found to enhance the efficiency of chemotherapy thereby reducing its side effects. Previous studies found that ginsenoside Rg3 can reduce the occurrence of NSCLC by inducing DNA damage. Yet, its anti-DNA damaging effects and mechanisms in tumor cells are still not fully understood. This study explored the effect of ginsenoside Rg3 on DNA repair and VRK1/P53BP1 signaling pathway. Ginsenoside Rg3 treatment significantly decreased the incidence and invasionin a mouse model of lung cancer induced by urethane. The results of cell survival assay and single cell gel electrophoresis showed that ginsenoside Rg3 protected lung adenocarcinoma cells from DNA damage as well as inhibited the proliferation of tumor cells. Ginsenoside Rg3 increased the mRNA and protein expression of VRK1 in NSCLC cells as measured by RT-qPCR and western blot, respectively. These findings suggests that ginsenoside Rg3 regulates VRK1 signaling. Immunofluorescence assays showed that P53BP1 and VRK1 protein level increased, and the VRK1 protein translocated between the nuclei and cytoplasm. Finally, this conclusion was confirmed by the reverse validation in VRK1-knockdown cells. Taken together, these results show that ginsenoside Rg3 upregulate VRK1 expression and P53BP1 foci formation in response to DNA damage thereby inhibiting the tumorigenesis and viability of cancer cells. These findings reveal the role of Rg3 in lung cancer and provides therapeutic targets for developing new drugs in the prevention and treatment of lung cancer.

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PMID: 

J Food Biochem. 2019 Sep 13:e13047. Epub 2019 Sep 13. PMID: 31515823

Abstract Title: 

Ameliorative effect of flaxseed (Linum usitatissimum) and its protein on ethanol-induced hepatotoxicity in Wistar rats.

Abstract: 

Hepatoprotective effect of flaxseed and its protein on ethanol-induced hepatotoxicity in adult Wistar rats was investigated. The rats were divided into eight groups of which two served as control (group I: Control for AIN-93M diet groups and group II: Control for cereal-pulse diet groups) and six groups received ethanol orally every day. After 10 days along with ethanol, the rats received AIN-93M diet (group III); AIN-93M diet and commercial hepatoprotective formulation (CHF) (group IV); casein replaced by flaxseed protein in AIN-93M diet (group V); cereal-pulse diet (group VI); cereal-pulse diet and CHF (group VII); cereal-pulse diet containing flaxseed (group VIII) for four weeks. The flaxseed and its protein significantly prevented the elevation of plasma markers of hepatic damage, lowered lipid peroxidation, mitigated changes in antioxidant enzymes, and suppressed histopathological signs of hepatic damage. The hepatoprotective effect of flaxseed and its protein was comparable to CHF. These findings implicate the ameliorative effect of flaxseed and its protein on ethanol-induced hepatotoxicity. PRACTICAL APPLICATIONS: Owing to globalization and an increase in earning capacity, alcohol consumption is becoming a part of sociallife and gradually transforming to addiction. Binge drinking is highly prevalent among low socioeconomic status population, which poses severe risks to health. Alcohol abuse is a public health problem causing three million deaths annually worldwide. Alcohol consumption is known to be a major causeof liver damage worldwide and has contributed to 44% of deaths from liver disease. As abstaining from alcohol is a challenging task, there is an escalating need to formulate potential hepatoprotective agents to prevent alcohol-induced hepatic damage. This study investigates the efficacy of flaxseedand its protein in conferring protection to the liver against ethanol-induced hepatotoxicity. This study also explores the benefits of incorporating flaxseed in the staple cereal-pulse diet. Findings of this study suggest that incorporation of flaxseed or its protein in food formulations can preventhepatotoxicity and improve the overall quality of life among alcoholics.

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PMID: 

Front Biosci (Schol Ed). 2020 Jan 1 ;12:38-56. Epub 2020 Jan 1. PMID: 31585864

Abstract Title: 

Anti-atherosclerotic and cardiovascular protective benefits of Brazilian nuts.

Abstract: 

Brazil nuts are rich in magnesium, selenium, arginine and other amino acids, dietary fiber, tocopherols (vitamin E), phytosterols, linoleic acid, linolenic acid, sitosterols, monounsaturated and polyunsaturated fatty acids, polyphenols and other amino acids. Due to such a rich mixture of nutrients, Brazil nuts protect LDL from peroxidation, and improve endothelial function, blood pressure, lipid metabolism, and decrease endothelial inflammatory markers, DNA oxidation, and blood lipids (cholesterol, LDL, triglycerides). Here, we review and propose biological mechanisms by which bioactive compounds of Brazil nuts afford protections against atherosclerosis and cardiovascular diseases. Just a few nutsprovide sufficient cardiovascular benefits, including protection against development and progression of atherosclerosis.

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PMID: 

Planta Med. 2019 Oct 11. Epub 2019 Oct 11. PMID: 31604353

Abstract Title: 

Pistacia Genus as a Potential Source of Neuroprotective Natural Products.

Abstract: 

Neuroprotective agents are able to defend the central nervous system against acute or chronic neuronal injuries. Even with the progress made over the last decades, most of the medications prescribed for the management of neurodegenerative diseases can only reduce their symptoms and slow down their progression. Based on natural product research, there are potential effective medicinal plants and phytochemicals for modulating neuronal functions and protecting against neurodegeneration. Plants in the genusare also among valuable natural resources for neuroprotection research based on experiences in traditional medicine. Studies have supported the value of bioactive compounds of the genusfor central nervous system disorders such as Alzheimer's, Parkinson's, multiple sclerosis, cerebral ischemia, depression, and anxiety. Related literature has also revealed that most of the evidence on neuroprotection in the genusis in the form of preliminary studies, mainly including models of behavior, motor function, and memory impairments in animals, neural toxicity, cerebral ischemia and seizure models, evaluation of their effects on antioxidant and inflammatory biomarkers, amyloidaggregation, and acetylcholinesterase as well as investigations into some cellular pathways. Along with the phytonutrients in kernels such as pistachios, various phytochemicals, mostly terpenes, and phenolic compounds have also been identified in different plant parts, in particular their oleoresins, of species in the genus. In this review, the pharmacology of neurological effects and related molecular mechanisms of the plants belonging to the genusand its active constituents, as well as pharmacokinetics aspects, are discussed.

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PMID: 

Appetite. 2019 Oct 8 ;144:104483. Epub 2019 Oct 8. PMID: 31604062

Abstract Title: 

Daily consumption of pistachios over 12 weeks improves dietary profile without increasing body weight in healthy women: A randomized controlled intervention.

Abstract: 

Dietary guidelines around the world recommend the regular intake of nuts because of their nutrient contribution to the diet and reported health benefits. However, consumers are often reluctant to include nuts in their diet due to the high caloric density of nuts. In a 12-week randomized, controlled intervention, we investigated how adding a pistachio portion to the daily diet affects body weight and composition, satiety, energy and nutrient intake. Sixty healthy pre-menopausal women who did not typically consume nuts were randomly assigned to a control or an experimental groups. Experimental participants (n = 30) consumed 44 g (250 kcal) pistachios mid-morning while controls (n = 30) maintained their current eating habits for 12 weeks. Ad libitum food intake and appetite sensations following the pistachio portion were assessed in all participants before and after the intervention in four 2-consecutive-day test sessions (under laboratory and then free-living conditions). Body weight and composition (DXA) were unchanged in both groups after 12 weeks. Pre- and post-intervention tests showed that ad libitum intake adjusted to the pistachio portion, mostly via reduced intakes of carbohydrates and starch, in parallel with decreased hunger and increased satiety following the morning snack. Intakes of MUFA, PUFA, linoleic acid, thiamin, pyridoxine, copper, manganese, and zinc were significantly higher among women consuming the pistachio snack, in spite of compensatory adjustments in intake. In conclusion, daily intake of 44 g pistachios improved nutrient intake without affecting body weight or composition in healthy women. The additional calories provided by the pistachios induced satiety and sufficient adjustment of intake to prevent body weight changes. CLINICAL TRIAL REGISTRY NUMBER: NCT03526120https://ift.tt/35SJ9qb.

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PMID: 

Antioxidants (Basel). 2019 Sep 9 ;8(9). Epub 2019 Sep 9. PMID: 31505827

Abstract Title: 

Particulate Matter 2.5 Mediates Cutaneous Cellular Injury by Inducing Mitochondria-Associated Endoplasmic Reticulum Stress: Protective Effects of Ginsenoside Rb1.

Abstract: 

The prevalence of fine particulate matter-induced harm to the human body is increasing daily. The aim of this study was to elucidate the mechanism by which particulate matter 2.5 (PM) induces damage in human HaCaT keratinocytes and normal human dermal fibroblasts, and to evaluate the preventive capacity of the ginsenoside Rb1. PMinduced oxidative stress by increasing the production of reactive oxygen species, leading to DNA damage, lipid peroxidation, and protein carbonylation; this effect was inhibited by ginsenoside Rb1. Through gene silencing of endoplasmic reticulum (ER) stress-related genes such as,,, and, and through the use of the ER stress inhibitor tauroursodeoxycholic acid (TUDCA), it was demonstrated that PM-induced ER stress also causes apoptosis and ultimately leads to cell death; however, this phenomenon was reversed by ginsenoside Rb1. We also found that TUDCA partially restored the production of ATP that was inhibited by PM, and its recovery ability was significantly higher than that of ginsenoside Rb1, indicating that the process of ER stress leading to cell damage may also occur via the mitochondrial pathway. We concluded that ER stress acts alone or via the mitochondrial pathway in the induction of cell damage by PM, and that ginsenoside Rb1 blocks this process. Ginsenoside Rb1 shows potential for use in skin care products to protect the skin against damage by fine particles.

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PMID: 

Diabetes Care. 2019 Oct 3. Epub 2019 Oct 3. PMID: 31582428

Abstract Title: 

Changes in Consumption of Sugary Beverages and Artificially Sweetened Beverages and Subsequent Risk of Type 2 Diabetes: Results From Three Large Prospective U.S. Cohorts of Women and Men.

Abstract: 

OBJECTIVE: We evaluated the associations of long-term changes in consumption of sugary beverages (including sugar-sweetened beverages and 100% fruit juices) and artificially sweetened beverages (ASBs) with subsequent risk of type 2 diabetes.RESEARCH DESIGN AND METHODS: We followed up 76,531 women in the Nurses' Health Study (1986-2012), 81,597 women in the Nurses' Health Study II (1991-2013), and 34,224 men in the Health Professionals' Follow-up Study (1986-2012). Changes in beverage consumption (in 8-ounce serving/day) were calculated from food frequency questionnaires administered every 4 years. Multivariable Cox proportional regression models were used to calculate hazard ratios for diabetes associated with changes in beverage consumption. Results of the three cohorts were pooled using an inverse variance-weighted, fixed-effect meta-analysis.RESULTS: During 2,783,210 person-years of follow-up, we documented 11,906 incident cases of type 2 diabetes. After adjustment for BMI and initial and changes in diet and lifestyle covariates, increasing total sugary beverage intake (including both sugar-sweetened beverages and 100% fruit juices) by>0.50 serving/day over a 4-year period was associated with a 16% (95% CI 1%, 34%) higher diabetes risk in the subsequent 4 years. Increasing ASB consumption by>0.50 serving/day was associated with 18% (2-36%) higher diabetes risk. Replacing one daily serving of sugary beverage with water, coffee or tea, but not ASB, was associated with a 2-10% lower diabetes risk.CONCLUSIONS: Increasing consumption of sugary beverages or ASBs was associated with a higher risk of type 2 diabetes, albeit the latter may be affected by reverse causation and surveillance bias.

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PMID: 

Biotech Histochem. 2019 Sep 11:1-9. Epub 2019 Sep 11. PMID: 31509032

Abstract Title: 

Royal jelly increased map-2 expression in hippocampal neurons of hypothyroid rats: an immunohistochemical study.

Abstract: 

We investigated microtubule-associated protein 2 (MAP-2) immunoreactivity of hippocampal neurons and the potential role of royal jelly (RJ) in regulating MAP-2 during experimental hypothyroidism (HT). Thirty adult female Wistar albino rats were randomized into five groups: the control group was untreated, the sham control group was treated with 10 mg/kg 0.9% sterile saline injected intraperitoneally (i.p.), The RJ group was treated with 100 mg/kg RJ by oral gavage, the HT group was treated with 10 mg/kg propylthiouracil (PTU) i.p. to induce experimental hypothyroidism, and the HT + RJ group was treated with 10 mg/kg PTU i.p. + 100 mg/kg RJ by oral gavage. Oral and i.p. administrations were performed once daily for 20 days. Thyroid stimulating hormone (TSH) and free thyroxine (fT4) levels in the serum were measured biochemically, MAP-2 was measured immunohistochemically in the hippocampus and an immunohistochemical H score was calculated. MAP-2 immunoreactivity appeared in the cytoplasm of neuron cell bodies and dendrites in the hippocampal CA3 and CA1 regions in the control, sham control and RJ groups. MAP-2 immunoreactivity decreased significiantly in the HT group compared to control, sham control and RJ groups. Also, vascular dilation and swollen cells were observed following PTU administration. The degeneration that was observed in the HT group decreased by RJ administration. By contrast, MAP-2 immunoreactivity increased following administration of RJ. Experimental hypothyroidism reduced significiantly MAP-2 immunoreactivity in both the CA3 and CA1 regions and caused degeneration, including edema and vascular dilation, in the hippocampus. RJ increased MAP-2 expression and exhibited a therapeutic effect on the degenerative changes.

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