PMID: 

Microorganisms. 2019 Dec 14 ;7(12). Epub 2019 Dec 14. PMID: 31847423

Abstract Title: 

Efficacy of Kombucha Obtained from Green, Oolong, and Black Teas on Inhibition of Pathogenic Bacteria, Antioxidation, and Toxicity on Colorectal Cancer Cell Line.

Abstract: 

Kombucha tea is a refreshing beverage that is produced from the fermentation of tea leaves. In this study, kombucha tea was prepared using 1% green tea, oolong tea, and black tea, and 10% sucrose with acetic acid bacteria and yeast. The pH values of the kombucha tea were found to be in a range of 2.70-2.94 at 15 days of fermentation. The lowest pH value of 2.70 was recorded in the kombucha prepared from black tea. The total acidity of kombucha prepared from black tea was the highest by 16.75 g/L and it was still maintained after heat treatment by boiling and after autoclaved. Six organic acids: glucuronic, gluconic, D-saccharic acid 1,4-lactone, ascorbic, acetic, and succinic acid in kombucha tea were detected by HPLC with the optimization for organic acids detection using isocratic elution buffer with C18 conventional column. The highest level of organic acid was gluconic acid. Kombucha prepared from green tea revealed the highest phenolic content and antioxidation against DPPH radicals by 1.248 and 2.642 mg gallic acid/mL kombucha, respectively. Moreover, pathogenic enteric bacteria:.O157:H7Typhi, andwere inhibited by kombucha and heat-denatured kombucha with diameter of the inhibition zones ranged from 15.0± 0.0-25.0 ± 0.0 mm. In addition, kombucha prepared from green tea and black tea demonstrated toxicity on Caco-2 colorectal cancer cells. Therefore, kombucha tea could be considered as a potential source of the antioxidation, inhibition of pathogenic enteric bacteria, and toxicity on colorectal cancer cells.

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PMID: 

Genetics. 2019 Dec 18. Epub 2019 Dec 18. PMID: 31852725

Abstract Title: 

Antioxidant CoQ10 Restores Fertility by Rescuing Bisphenol A-Induced Oxidative DNA Damage in theGermline.

Abstract: 

Endocrine-disrupting chemicals are ubiquitously present in our environment, but the mechanisms by which they adversely affect human reproductive health and strategies to circumvent their effects remain largely unknown. Here we show in, that supplementation with the antioxidant Coenzyme Q10 (CoQ10) rescues the reprotoxicity induced by the widely used plasticizer and endocrine disruptor bisphenol A (BPA) in part by neutralizing DNA damage resulting from oxidative stress. CoQ10 significantly reduces BPA-induced elevated levels of germ cell apoptosis, phosphorylated checkpoint kinase 1 (CHK-1), double-strand breaks (DSBs) and chromosome defects in diakinesis oocytes. BPA-induced oxidative stress, mitochondrial dysfunction, and increased gene expression of antioxidant enzymes in the germline are counteracted by CoQ10. Finally, CoQ10 treatment also reduced the levels of aneuploid embryos and BPA-induced defects observed in early embryonic divisions. We propose that CoQ10 may counteract BPA-induced reprotoxicity through the scavenging of reactive oxygen species and free radicals and that this natural antioxidant could constitute a low-risk and low-cost strategy to attenuate the impact on fertility by BPA.

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PMID: 

Exp Ther Med. 2020 Jan ;19(1):33-44. Epub 2019 Nov 13. PMID: 31853270

Abstract Title: 

Bisphenol A-induced oxidative damage in the hepatic and cardiac tissues of rats: The modulatory role of sesame lignans.

Abstract: 

Bisphenol A (BPA) is an environmental pollutant that is widely produced throughout the world. It is primarily used in the manufacture of polycarbonate plastics, epoxy resins, paints and dental materials. BPA has been reported to promote hepatotoxicity and cardiotoxicity. The antioxidant activity of sesame lignans is well established. The current study assessed the protective efficiency of sesame lignans against BPA-induced hepatotoxicity and cardiotoxicity. Rats were divided into 4 groups: A control group, a BPA-treated group, a sesame lignans-treated group and a sesame lignans and BPA-treated group. Rats were orally administered their respective doses daily [30 mg/kg body weight (BW) BPA and/or 20 mg/kg BW sesame lignans] for 6 weeks. Liver function tests were performed using serum of all groups. Lipid profile and antioxidant status were also measured in liver tissue of the studied groups. The results were confirmed by histopathological examination of liver and heart tissues. The oral administration of BPA was revealed to elicit significant decreases in the activities of hepatic glutathione peroxidase, glutathione reductase, superoxide dismutase and glutathione. It also significantly increased levels of malondialdehyde. Furthermore, BPA-treatment resulted in lipid accumulation, elevated activities of alanine aminotransferase, creatine kinase MB and lactate dehydrogenase, and histological changes of liver and heart tissues. However, the co-administration of sesame lignans and BPA attenuated hepatotoxicity, cardiotoxicity and BPA-induced histological changes. The results of the current study indicated that sesame lignans may be helpful in the development of novel natural drugs to treat hepatic and cardiovascular disorders.

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PMID: 

Environ Toxicol. 2019 Dec 10. Epub 2019 Dec 10. PMID: 31820560

Abstract Title: 

Bisphenols B, E, F, and S and 4-cumylphenol induce lipid accumulation in mouse adipocytes similarly to bisphenol A.

Abstract: 

Bisphenol A (BPA) has been widely reported to exert endocrine disrupting effects, including the induction of adipogenesis in cultured preadipocytes and intact animals. Because of the potential harm to human health, BPA is being substituted by structurally related bisphenols. Whether or not such BPA analogues are safe substitutes, however, remains largely unknown. Here, we investigated the potential of bisphenol B (BPB), bisphenol E (BPE), bisphenol F (BPF), bisphenol S (BPS), and 4-cumylphenol (4-CP) to affect lipid and hormone levels in 3 T3-L1 cells. We found that BPB, BPE, BPF, BPS, and 4-CP all affected lipid accumulation and leptin levels to the same extent and potencies as BPA. Based on these and other results, we conclude that these BPA analogues and 4-CP most likely will elicit similar effects on adipocytes as BPA. Using them to substitute BPA in products should be done with caution.

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PMID: 

Food Funct. 2019 Jul 17 ;10(7):3828-3838. PMID: 31187840

Abstract Title: 

Monofloral honey from a medical plant, Prunella Vulgaris, protected against dextran sulfate sodium-induced ulcerative colitis via modulating gut microbial populations in rats.

Abstract: 

Honeys produced from medicinal plants hold great promise for human health. Herein, we determined the chemical composition and gastrointestinal protective effects of a novel monofloral honey from Prunella vulgaris (PVH). The physicochemical parameters (moisture, sugars, pH, protein content, diastase activity, and hydroxymethylfurfural) of the PVH samples met the criteria specified in European Union regulations and Chinese National Standards. Fifteen phenolic compounds were identified and quantified via high-performance liquid chromatography with a diode array detector and with time of flight tandem mass spectrometry detection (HPLC-DAD/Q-TOF-MS). Rosmarinic acid was found to be a potential marker for PVH identification. Using a dextran sulfate sodium (DSS)-induced acute colitis model, we demonstrated that the administration of PVH (5 g per kg b.w., p.o.) significantly decreased the disease activity index and mitigated colonic histopathological changes in rats. PVH also modulated the gut microbiota composition in the colitic rats, reversing the increase in the Bacteroidetes/Firmicutes ratio and restoring Lactobacillus spp. populations in DSS-challenged rats. The results of this study provide fundamental data on PVH, supporting its future application in the prevention of colitis.

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PMID: 

Free Radic Biol Med. 2019 Dec 5. Epub 2019 Dec 5. PMID: 31811921

Abstract Title: 

Protective effect of Prunella vulgaris var. L extract against blue light induced damages in ARPE-19 cells and mouse retina.

Abstract: 

Age-related macular degeneration (AMD) is one of leading causes that induce severe visual impairment and loss in the elderly. Previous studies have suggested that blue light (BL) could induce retinal degeneration, which is a major cause of the onset and development of severe AMD. In the retinal pigment epithelium (RPE) cells, A2E, a lipofuscin fluorophore, is accumulated with aging. When A2E is exposed to BL, it is easily oxidized to A2E-epoxides, leading to oxidative stress and inflammatory response in retina. The aim of this study was to investigate protective effect of Prunella vulagris (P.V) extract against oxidative stress and inflammation caused by BL, and to elucidate the underlying mechanisms in the cultured RPE cells and balb-c mice. In both model studies, P.V extract activated NF-E2 related factor 2 (Nrf-2)/hemeoxygenase-1 (HO-1) signaling pathway, followed by inhibition of ROS/MDA production, GSH depletion and reduction in SOD activity. Furthermore, P.V extract inhibited upregulation of inflammatory related genes (interlukin (IL)-1beta, IL-6, monocyte chemoattractant protein-1 (MCP-1), vascular endothelial growth factor A (VEGF A)) and BL induced RPE cell death, determined by cell viability and histological analyses. The mechanism of protection against inflammation by P.V extract involves inhibition of nuclear translocation of nuclear factor kappa beta (NF-kB) along with degradation of NF-kB inhibitor alpha (IkB alpha). The results suggest that P.V extract could be a potential intervention to prevent the onset and development of severe AMD.

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PMID: 

Antioxidants (Basel). 2019 Dec 5 ;8(12). Epub 2019 Dec 5. PMID: 31817413

Abstract Title: 

Anti-Atherosclerotic Effect ofLeaf Polyphenols against Tumor Necrosis Factor-alpha-Induced Abnormal Vascular Smooth Muscle Cell Migration and Proliferation.

Abstract: 

The proliferation and migration of vascular smooth muscle cells (VSMCs) are major events in the development of atherosclerosis following stimulation with proinflammatory cytokines, especially tumor necrosis factor-alpha (TNF-α). Plant-derived polyphenols have attracted considerable attention in the prevention of atherosclerosis.leaf has been showed to inhibit endothelial cell oxidative injury, low-density lipoprotein oxidation, and foam cell formation. In this study, we examined the anti-atherosclerotic effect ofleaf polyphenols (HLPs) against abnormal VSMC migration and proliferation in vitro and in vivo. Firstly, VSMC A7r5 cells pretreated with TNF-α were demonstrated to trigger abnormal proliferation and affect matrix metalloproteinase (MMP) activities. Non-cytotoxic doses of HLPs abolished the TNF-α-induced MMP-9 expression and cell migration via inhibiting the protein kinase PKB (also known as Akt)/activator protein-1 (AP-1) pathway. On the other hand, HLP-mediated cell cycle G0/G1 arrest might be exerted by inducing the expressions of p53 and its downstream factors that, in turn, suppress cyclin E/cdk2 activity, preventing retinoblastoma (Rb) phosphorylation and the subsequent dissociation of Rb/E2F complex. HLPs also attenuated reactive oxygen species (ROS) production against TNF-α stimulation. In vivo, HLPs improved atherosclerotic lesions, and abnormal VSMC migration and proliferation. Our data present the first evidence of HLPs as an inhibitor of VSMC dysfunction, and provide a new mechanism for its anti-atheroscleroticactivity.

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PMID: 

Phytother Res. 2019 Dec 12. Epub 2019 Dec 12. PMID: 31833112

Abstract Title: 

Effect of Hibiscus sabdariffa (Roselle) supplementation in regulating blood lipids among patients with metabolic syndrome and related disorders: A systematic review and meta-analysis.

Abstract: 

This study aimed to assess the efficacy of Hibiscus sabdariffa (Roselle) in regulating blood lipids among patients with metabolic syndrome and related disorders. PubMed, the Cochrane Library, Embase, Web of Science, and Clinical Trials were searched to identify the randomised controlled trials meeting the inclusion criteria. Study selection, data extraction, and risk assessment were performed according to Cochrane handbook; available data were analysed using STATA 15.0 software. Eventually, nine trials involving 503 participants were included in this meta-analysis. The results showed that compared with the control group, H. sabdariffa supplementation could reduce total cholesterol (WMD = -14.66; 95% CI [-18.22, -11.10]; p = .000; I= 46.9%) and low-density lipoprotein cholesterol (WMD = -9.46; 95% CI [-14.93, -3.99]; p = .001; I= 50.1%) but could not effectively reduce triglyceride (WMD = -0.77; 95% CI [-7.87, 6.33]; p = 0.832; I= 0%). Meanwhile, there were no serious adverse reactions reported in the included studies. To summarise, current evidence suggests that the benefits of H. sabdariffa supplementation to patients with metabolic diseases are associated with its cholesterol-lowering effects; however, more high-quality clinical trials are needed to confirm these results.

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PMID: 

Aging Cell. 2019 Nov 24:e13076. Epub 2019 Nov 24. PMID: 31762202

Abstract Title: 

Extra virgin olive oil improves synaptic activity, short-term plasticity, memory, and neuropathology in a tauopathy model.

Abstract: 

In recent years, increasing evidence has accumulated supporting the health benefits of extra virgin olive oil (EVOO). Previous studies showed that EVOO supplementation improves Alzheimer's disease (AD)-like amyloidotic phenotype of transgenic mice. However, while much attention has been focused on EVOO-mediated modulation of Aβ processing, its direct influence on tau metabolism in vivo and synaptic function is still poorly characterized. In this study, we investigated the effect of chronic supplementation of EVOO on the phenotype of a relevant mouse model of tauopathy, human transgenic tau mice (hTau). Starting at 6 months of age, hTau mice were fed chow diet supplemented with EVOO or vehicle for additional 6 months, and then the effect on their phenotype was assessed. At the end of the treatment, compared with control mice receiving EVOO displayed improved memory and cognition which was associated with increased basal synaptic activity and short-term plasticity. This effect was accompanied by an upregulation of complexin 1, a key presynaptic protein. Moreover, EVOO treatment resulted in a significant reduction of tau oligomers and phosphorylated tau at specific epitopes. Our findings demonstrate that EVOOdirectly improves synaptic activity, short-term plasticity, and memory while decreasing tau neuropathology in the hTau mice. These results strengthen the healthy benefits of EVOO and further support the therapeutic potential of this natural product not only for AD but also for primary tauopathies.

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