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PMID: 

Int J Biol Macromol. 2019 Jun 28 ;137:139-150. Epub 2019 Jun 28. PMID: 31260772

Abstract Title: 

Preparation of Chlorella vulgaris polysaccharides and their antioxidant activity in vitro and in vivo.

Abstract: 

In the present study, six different polysaccharides (RFPs, MAPs, UWPs, AEPs, HWPs and CEPs) were extracted from Chlorella vulgaris using repeated freeze-thawing, microwave-assisted-, ultrasonic wave-, alkali-, hot water-, and cellulase-based methods; and antioxidant property assays were performed both in vitro and in vivo. Radical-scavenging capacity (using DPPH, superoxide and hydroxyl radicals) and metal chelating ability were assessed in vitro; Caenorhabditis elegans was used to assess antioxidant effects in vivo. Based on the in vitro screening tests, UWPs exhibited high antioxidant capacity. The UWP yield was 17.1% ± 2.2%; the DPPH-, superoxide-, and hydroxyl radical-scavenging rates were 65.1% ± 2.4%, 61.2% ± 2.7%, and 56.2% ± 2.2%, respectively, and the metal chelating ability was 63.6% ± 2.5% at a concentration of 0.4 mg/mL. UWPs also exhibited high antioxidant activity in vivo.UWPs significantly increased the lifespan of C. elegans under oxidative stress induced by hydrogen peroxide compared with the control group, enhanced stress-resistance-related enzymes, including catalase and superoxide dismutase by 7.29% ± 1.8% and 24.41% ± 4.8%, respectively. The resultsof the present study indicate that the extraction methods of C. vulgaris polysaccharides were a key factor influencing antioxidant activity.

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PMID: 

FEBS Open Bio. 2019 Jun ;9(6):1082-1096. Epub 2019 Apr 20. PMID: 31006177

Abstract Title: 

Blueberry juice protects osteocytes and bone precursor cells against oxidative stress partly through SIRT1.

Abstract: 

Oxidative stress and abnormal osteocyte apoptosis are often related to dysregulation of bone turnover and chronic bone loss, and so fruit and vegetables with high antioxidant potential may play an important role in the prevention and/or management of osteoporosis. Osteocytes are the main regulators of bone remodelling. For the first time, we demonstrate here that blueberry juice (BJ), obtained from Vaccinium myrtillus, rich in polyphenols, shows antioxidant and antiosteoclastogenic properties in MLO-Y4 osteocytes. We report that BJ prevents oxidative stress-induced apoptosis and reverses the increase in receptor activator of nuclear factorκB ligand and sclerostin expression, crucial factors for osteoclast activation and bone resorption. BJ is also able to prevent oxidative stress-induced cell cytotoxicity in bone marrow mesenchymal stromal cells (MSCs), which are considered to be an important tool for cell therapy in bone disorders.No significant difference in preventing these events was observed between BJ and blueberry dry extract containing equal amounts of total soluble polyphenols. We have also shown that blueberry acts as both an antioxidant and an activator of sirtuin type 1, a class III histone deacetylase involved incell death regulation and considered a molecular target for blocking bone resorption without affecting osteoclast survival. Overall, these novel data obtained in osteocytes and MSCs may help us clarify the mechanisms by which blueberry counteracts oxidative stress-induced damage in bone remodellingand osteogenesis at the cellular and molecular level. Our findings are consistent with the reported beneficial effects of blueberry on bone tissue reported in animal studies, which suggest that blueberry may be a useful supplement for the prevention and/or management of osteoporosis and osteogenicprocess.

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PMID: 

Food Funct. 2019 Jun 19 ;10(6):3430-3438. PMID: 31134999

Abstract Title: 

Bilberry anthocyanin improves the serum cholesterol in aging perimenopausal rats via the estrogen receptor signaling pathway.

Abstract: 

With aging, there is an increasing risk for women to develop perimenopause syndrome, which is harmful to women's physical and mental health. The present study investigated the health benefits of bilberry anthocyanin (BA) on aging perimenopausal Sprague-Dawley rats. Rats that entered into perimenopause through natural aging were treated for 8 weeks with BA, and received either a low dose (LD, 35 mg per kg of bodyweight), medium dose (MD, 70 mg per kg of bodyweight), or high dose (HD, 140 mg per kg of bodyweight). The experimental results suggested that all three dosages of BA, especially the high dose, significantly reduced the serum total cholesterol (TC), triglyceride (TG) and low density lipoprotein cholesterol (LDL-C) levels. In addition, BA supplementation markedly reduced the serum malondialdehyde (MDA), effectively increased the activity of hepatic total superoxide dismutase (T-SOD), significantly raised the high density lipoprotein cholesterol (HDL-C), increased the number of estrogen receptors, and effectively up-regulated the expression levels of G protein-coupled receptor 30 (GPR30), protein kinase B (AKT), and extracellular regulated protein kinase 2 (ERK2). In summary, BA has a great effect on improving the serum cholesterol in natural aging perimenopausal rats via the estrogen receptor signaling pathway, and it may be used as a dietary supplement for perimenopause women to decrease the risk of cardiovascular disease.

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PMID: 

Nutrients. 2019 Jun 15 ;11(6). Epub 2019 Jun 15. PMID: 31208043

Abstract Title: 

Dietary Fiber in Bilberry Ameliorates Pre-Obesity Events in Rats by Regulating Lipid Depot, Cecal Short-Chain Fatty Acid Formation and Microbiota Composition.

Abstract: 

Obesity is linked to non-alcoholic fatty liver disease and risk factors associated to metabolic syndrome. Bilberry () that contains easily fermentable fiber may strengthen the intestinal barrier function, attenuate inflammation and modulate gut microbiota composition, thereby prevent obesity development. In the current study, liver lipid metabolism, fat depot, cecal and serum short-chain fatty acids (SCFAs) and gut microbiome were evaluated in rats fed bilberries in a high-fat (HFD + BB) or low-fat (LFD + BB) setting for 8 weeks and compared with diets containing equal amount of fiber resistant to fermentation (cellulose, HFD and LFD). HFD fed rats did not obtain an obese phenotype but underwent pre-obesity events including increased liver index, lipid accumulation and increased serum cholesterol levels. This was linked to shifts of cecal bacterial community and reduction of major SCFAs. Bilberry inclusion improved liver metabolism and serum lipid levels. Bilberry inclusion under either LFD or HFD, maintained microbiota homeostasis, stimulated interscapular-brown adipose tissue depot associated with increased mRNA expression of uncoupling protein-1; enhanced SCFAs in the cecum and circulation; and promoted butyric acid and butyrate-producing bacteria. These findings suggest that bilberry may serve as a preventative dietary measure to optimize microbiome and associated lipid metabolism during or prior to HFD.

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PMID: 

Biosci Biotechnol Biochem. 2019 Jun 27:1-11. Epub 2019 Jun 27. PMID: 31244392

Abstract Title: 

Extracts of bilberry (L.) fruits improve liver steatosis and injury in mice by preventing lipid accumulation and cell death.

Abstract: 

Bilberry has been reported to have anti-oxidant and anti-inflammatory properties. We studied the effect of bilberry (L.) fruits extracts (BEs) on the pathogenesis caused by lipid accumulation in fatty liver and non-alcoholic steatohepatitis (NASH). 5μg/ml of BEs was enough to suppress lipid accumulation in the fatty liver model of the mouse hepatic AML12 cells. BEs increased cell viability and anti-oxidant capacity, presumably by activating (phosphorylating) Akt/STAT3 and inducing MnSOD/catalase. BEs also significantly reduced Rubicon and induced p62/SQSTM1, possibly contributing to reduce cellular lipids (lipophagy). When the mice were fed supplemented with BEs (5% or 10%, w/w), hepatic steatosis, injury, and hypercholesterolemia/hyperglycemia were significantly improved. Furthermore, histological and cytokine studies indicated that BEspossibly suppress hepatic inflammation (hepatitis) and fibrosis. Therefore, BEs improved liver steatosis and injury, and potentially suppress fibrosis by suppressing inflammatory response, which therefore may prevent the progression of fatty liver to NASH.

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PMID: 

Environ Toxicol. 2019 Jul 9. Epub 2019 Jul 9. PMID: 31287222

Abstract Title: 

Impact of gestational low protein diet and postnatal bisphenol A exposure on chemically induced mammary carcinogenesis in female offspring rats.

Abstract: 

This study evaluated the effect of gestational low protein diet (LPD) and/or postnatal bisphenol A (BPA) exposure on mammary gland development and carcinogenesis in female offspring. Pregnant Sprague-Dawley rats were fed a normal protein diet (NPD, 17% protein) or LPD (6% protein). At weaning, female offspring were distributed in four groups (NPD, LPD, NPD + BPA, and LPD + BPA) and received vehicle or BPA in drinking water (0.1%), during postnatal day (PND) 21 to 51. On PND 51, some female offspring were euthanized or received a single dose of 7,12-dimethylbenzoanthracene (DMBA, 30 mg/kg, i.g.) and were euthanized on PND 250. On PND 51, neither gestational LPD nor postnatal BPA exposure, individually or in combination, significantly altered the development of mammary gland tree, mean number of terminal structures or estrogen receptor beta (ER-β), proliferating cell nuclear antigen (PCNA) or caspase-3 protein expression in the mammarytissue. A significant reduction in mammary epithelial area (%) was observed in both LPD groups and a significant increase in ER-α protein expression was detected only in LPD group. In LPD + BPA group was observed a significant increase in both fat pad area (%) and in mean number of mammary epithelial cells positive for progesterone receptor (PR). On PND 250, the groups that received BPA presented lower latency and higher tumor incidence and tumor multiplicity and LPD + BPA group more aggressive tumors. These findings suggest that postnatal BPA exposure associated with gestational LPDis able to induce morphological changes in the mammary gland and increase susceptibility to mammary carcinogenesis.

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PMID: 

Environ Sci Pollut Res Int. 2019 Jul 9. Epub 2019 Jul 9. PMID: 31286379

Abstract Title: 

Exposure to bisphenol A and diabetes risk in Mexican women.

Abstract: 

Bisphenol A (BPA) is an endocrine-disrupting chemical widely used in the production of polycarbonate plastics and epoxy resins, which has been previously linked to diabetes among non-Hispanic populations. As part of a case control study for breast cancer, only controls with BPA information were included in this report. The final sample size comprises 70 self-reported diabetics and 334 non-diabetics. Urinary free bisphenol A (BPA-F) (μg/L) was determined by solid-phase extraction and HPLC/FLD analysis. Logistic regression models were used to evaluate the association between BPA-F and self-reported diabetes. After adjusting by age, urinary BPA-F (4.06-224.53 μg/g creatinine) was associated with diabetes exposure (OR = 1.85;95% CI 1.04, 3.28) compared with women in the reference category (0.67-4.05 μg/g creatinine). BPA may be an environmental cofactor of diabetes. More studies are needed to confirm this result, especially in Hispanic populations.

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PMID: 

Toxicol Rep. 2019 ;6:578-589. Epub 2019 Jun 17. PMID: 31293903

Abstract Title: 

Gallic acid protects rat liver mitochondriafrom bisphenol A induced oxidative stress mediated damages.

Abstract: 

Humans are often exposed to bisphenol A (BPA), the monomer of polycarbonate plastics and epoxy resins, through BPA contaminated drinking water, beverages and foods, packaged in polycarbonate plastic bottles and cans coated with epoxy resins due to leaching. Several research groups have reported that BPA may cause damage of mitochondria in liver, kidney, heart and brain cells by inducing oxidative stress. The antioxidant efficacy of gallic acid (GA), a polyphenol compound obtained from plants, against different toxicants induced oxidative stress has been well established. The aim of the present study was to examine the protective efficacy of GA against BPA induced oxidative damages of the rat liver mitochondria. In our study, we have found a significant decrease in the intactness of mitochondria; a significant increase () in the levels of lipid peroxidation end product (i.e. malondialdehyde) and protein carbonylation product; and also a significant decrease () in the reduced glutathione content; when mitochondria were incubated with BPA (160μM/ml) only. These results indicate that BPA probably causes damage to the cellular macromolecules through oxidative stress. We have observed significant counteractions () against BPA induced alterations in mitochondrial intactness, lipid peroxidation and protein carbonylation products formation and reduced glutathione content when mitochondria were incubated with BPA and GA (20 μg/ml/ 40 μg/ml/ 80 μg/ml) in combination in a dose-dependent manner. Gallic acid also showed significant restorations () of the activities of antioxidant enzymes, Krebs cycle enzymes, respiratory chain enzymes and thiolase when mitochondria were incubated with BPA and dosage of GA (20 μg/ml/ 40 μg/ml/ 80 μg/ml) in combination compared to BPA incubated mitochondria. Furthermore, GA significantly () counteracted the BPA induced decrease in tryptophan and NADH auto-fluroscence levels in mitochondria. This result suggests that GA protects the mitochondria probably by reducing the oxidative stress. Besides, GA protects the mitochondrial surface from BPA induced oxidative damages as viewed under the scanning electron microscope. Considering all the results, it can be concluded that GA shows potent efficacy in protecting the rat liver mitochondriafrom BPA induced oxidative stress mediated damages.

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