PMID: 

Biomarkers. 2019 Aug 5:1-7. Epub 2019 Aug 5. PMID: 31305161

Abstract Title: 

Protective effects of betanin against paracetamol and diclofenac induced neurotoxicity and endocrine disruption in rats.

Abstract: 

Overconsumption of paracetamol (PAR) and diclofenac (DF) have been reported to induce neurotoxicity and endocrine disruption.The current study was designed to explore the protective potential of betanin against PAR and DF inducing neurotoxicity and endocrine disruption in a rat model.Forty rats were equally divided into five groups: group I served as control, group II received PAR (400 mg/kg), group III received PAR plus betanin (25 mg/kg), group IV received DF (10 mg/kg) and group V received DF plus betanin orally for 28 consecutive days. Thyroid axis hormones, sex hormone, neurotransmitters, paraoxonase-1, hemeoxygenase-1 and nuclear factor-2 were measured by ELISA. While, the oxidative stress markers were colorimetrically estimated. Moreover, DNA damage and histopathological picture of the brains were investigated.A marked reduction in thyroid axis hormones, brain neurotransmitters and serum testosterone as well as enhanced oxidative stress and brain DNA damage accompanied by drastic changes in the brain histopathological picture were recorded in the challenged PAR and DF groups. Betanin supplementation ameliorated most of the biochemical and histopathological changes induced by PAR or DF.The study suggests betanin of potential protective effects against neurotoxicity and endocrine disruption induced by PAR and DF overconsumption.

read more

PMID: 

Nutrients. 2019 Aug 28 ;11(9). Epub 2019 Aug 28. PMID: 31466334

Abstract Title: 

Impact of Oral Intake of Glucosylceramide Extracted from Pineapple on Xerostomia: A Double-Blind Randomized Cross-Over Trial.

Abstract: 

The aim of this double-blind randomized cross-over trial was to evaluate the effect of oral intake of glucosylceramide extracted from pineapple on oral moisture and xerostomia symptoms.Sixteen participants who had xerostomia symptoms were randomly allocated into two groups. One group received, as test samples, tablets containing glucosylceramide extracted from pineapple (GCP) followed by placebo tablets. The other group received the test samples in the reverse order. Participants were instructed to take tablets of the first test sample once a day (after breakfast) for two consecutive weeks. Then, after a washout period of four weeks, participants were instructed to take the other test sample for two consecutive weeks. The oral moisture level of the lingual mucosa, xerostomia symptoms, and the number of fungiform papillae was evaluated.The oral moisture significantly increased, and the visual analog scale (VAS) of"How is the dryness of your mouth?"significantly improved after GCP tablets intake and not after placebo tablets intake. The number of fungiform papillae was not significantly different following the intake of GCP tablets or placebo tablets.Results suggested that oral intake of GCP may improve the moisture level and xerostomia symptoms.

read more

PMID: 

Nutrients. 2019 Aug 22 ;11(9). Epub 2019 Aug 22. PMID: 31443409

Abstract Title: 

Short-Term Betanin Intake Reduces Oxidative Stress in Wistar Rats.

Abstract: 

Oxidative stress is a common condition described in risk factors for cardiovascular disease. Betanin, a bioactive pigment from red beetroot demonstrates anti-inflammatory and antioxidant properties. The main aim of this study was to evaluate the short-term intake of betanin against oxidative stress in a rodent model, a common condition described in several risk factors for cardiovascular disease. Oxidative stress was induced in Wistar rats by a hyperlipidemic diet for 60 days, followed by betanin administration (20 mg·kg) through oral gavage for 20 days. Plasma biochemical parameters and antioxidant enzyme activities were evaluated. Lipid peroxidation and histopathological changes were determined in the liver. The hyperlipidemic diet caused hyperglycemia, hyperinsulinemia, insulin resistance, and increases in alanine transaminase and aspartate transaminase levels. Oxidative stress status was confirmed by reduction of antioxidant enzyme activities, increased lipid peroxidation, and liver damage. Purified betanin regulated glucose levels, insulin, and insulin resistance. Hepatic damage was reversed as evidenced by the reduction in alanine transaminase and aspartate transaminase levels and confirmed by histological analyses. Betanin reduced hepatic malondialdehyde and increased superoxide dismutase, catalase, and glutathione peroxidase activities. Short-term betanin intake modulated biochemical parameters, reversed hepatic tissue damage, and attenuated oxidative stress in Wistar rats.

read more

PMID: 

Exp Cell Res. 2011 Oct 1 ;317(16):2231-8. Epub 2011 Jul 20. PMID: 21787768

Abstract Title: 

Hepatic response to aluminum toxicity: dyslipidemia and liver diseases.

Abstract: 

Aluminum (Al) is a metal toxin that has been implicated in the etiology of a number of diseases including Alzheimer's, Parkinson's, dialysis encephalopathy, and osteomalacia. Al has been shown to exert its effects by disrupting lipid membrane fluidity, perturbing iron (Fe), magnesium, and calcium homeostasis, and causing oxidative stress. However, the exact molecular targets of aluminum's toxicity have remained elusive. In the present review, we describe how the use of a systems biology approach in cultured hepatoblastoma cells (HepG2) allowed the identification of the molecular targets of Al toxicity. Mitochondrial metabolism is the main site of the toxicological action of Al. Fe-dependent and redox sensitive enzymes in the tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS) are dramatically decreased by Al exposure. In an effort to compensate for diminished mitochondrial function, Al-treated cells stabilize hypoxia inducible factor-1α (HIF-1α) to increase ATP production by glycolysis. Additionally, Al toxicity leads to an increase in intracellular lipid accumulation due to enhanced lipogenesis and a decrease in the β-oxidation of fatty acids. Central to these effects is the alteration of α-ketoglutarate (KG) homeostasis. InAl-exposed cells, KG is preferentially used to quench ROS leading to succinate accumulation and HIF-1α stabilization. Moreover, the channeling of KG to combat oxidative stress leads to a reduction of l-carnitine biosynthesis and a concomitant decrease in fatty acid oxidation. The fluidity and interaction of these metabolic modules and the implications of these findings in liver-related disorders are discussed herein.

read more

PMID: 

Eur J Epidemiol. 2019 Aug 7. Epub 2019 Aug 7. PMID: 31392470

Abstract Title: 

Green tea consumption and mortality in Japanese men and women: a pooled analysis of eight population-based cohort studies in Japan.

Abstract: 

The aim of our study was to assess the association between green tea consumption and all-cause and cause-specific mortality in a pooled analysis of eight Japanese population-based cohort studies. Pooled hazard ratios (HR) and 95% confidence intervals (CI), derived from random effects models, were used to evaluate the associations between green tea consumption, based on self-report at baseline, and risk of all-cause and cause-specific mortality. During a mean follow-up of 17.3 years, among 313,381 persons, 52,943 deaths occurred. Compared with individuals who consumed

read more

PMID: 

Nutrients. 2019 Aug 29 ;11(9). Epub 2019 Aug 29. PMID: 31470581

Abstract Title: 

Korean Red Ginseng Extract Increases Apoptosis by Activation of the Noxa Pathway in Colorectal Cancer.

Abstract: 

BACKGROUND: Although the anticancer activity of Korean Red Ginseng (KRG) has been known in various cancers, the mechanism of KRG-induced apoptosis is unknown in colorectal cancer (CRC). In our study, we examined whether KRG induces apoptosis in CRC cells.METHODS: In the cell viability assay, the concentration of the appropriate KRG extracts was fixed at 2.5 mg/mL in numerous CRC cells. This fixed concentration was in other experiments, and it was confirmed that the KRG extracts induce apoptosis in CRC cells.RESULTS: We found that KRG induced Noxa activation and apoptosis and increased endoplasmic reticulum stress via reactive oxygen species production. This indicated that KRG efficiently enhanced cell death in CRC cells.CONCLUSION: Our results show that KRG can be used as a possible anticancer drug for patients with CRC.

read more

PMID: 

Nutrients. 2019 Aug 9 ;11(8). Epub 2019 Aug 9. PMID: 31405071

Abstract Title: 

Epigallocatechin-3-Gallate (EGCG) Suppresses Pancreatic Cancer Cell Growth, Invasion, and Migration partly through the Inhibition of Akt Pathway and Epithelial-Mesenchymal Transition: Enhanced Efficacy when Combined with Gemcitabine.

Abstract: 

Most pancreatic cancers are usually diagnosed at an advanced stage when they have already metastasized. Epigallocatechin-3-gallate (EGCG), a major polyphenolic constituent of green tea, has been shown to reduce pancreatic cancer growth, but its effect on metastasis remains elusive. This study evaluated the capacity of EGCG to inhibit pancreatic cancer cell migration and invasion and the underlying mechanisms. EGCG reduced pancreatic cancer cell growth, migration, and invasion in vitro and in vivo. EGCG prevented"Cadherin switch"and decreased the expression level of TCF8/ZEB1,β-Catenin, and Vimentin. Mechanistically, EGCG inhibited the Akt pathway in a time-dependent manner, by suppressing IGFR phosphorylation and inducing Akt degradation. Co-treatment with catalase or N-Acetyl-L-cysteine did not abrogate EGCG's effect on the Akt pathway or cell growth. Moreover, EGCG synergized with gemcitabine to suppress pancreatic cancer cell growth, migration, and invasion, through modulating epithelial-mesenchymal transition markers and inhibiting Akt pathway. In summary, EGCG may prove beneficial to improve gemcitabine sensitivity in inhibiting pancreatic cancer cell migration and invasion, to some extent through the inhibition of Akt pathway and epithelial-mesenchymal transition.

read more

PMID: 

Cancer Causes Control. 2019 Aug 26. Epub 2019 Aug 26. PMID: 31452000

Abstract Title: 

Green tea consumption and risk of hematologic neoplasms: the Japan Collaborative Cohort Study for Evaluation of Cancer Risk (JACC Study).

Abstract: 

PURPOSE: Experimental studies suggested that green tea may have an anticancer effect on hematologic neoplasms. However, few prospective studies have been conducted.METHODS: A total of 65,042 individuals aged 40-79 years participated in this study and completed a self-administered questionnaire about their lifestyle and medical history at baseline (1988-1990). Of these, 52,462 individuals living in 24 communities with information on incident hematologic neoplasms available in the cancer registry, who did nothave a history of cancer and provided valid information on frequency of green tea consumption, were followed through 2009. Hazard ratios (HRs) and 95% confidence intervals (CIs) for the incidence of hematologic neoplasms according to green tea consumption were analyzed.RESULTS: The incidence of hematologic neoplasms during a median follow-up of 13.3 years was 323. Compared with the never-drinkers of green tea, the multivariate HRs and 95% CIs for total hematologic neoplasms in green tea drinkers of ≤ 2 cups/day, 3-4 cups/day, and ≥ 5 cups/day were 0.65 (0.42-1.00), 0.73 (0.47-1.13), and 0.63 (0.42-0.96), respectively. The association wasmore prominent for acute myeloid leukemias and follicular lymphomas.CONCLUSIONS: The present cohort study suggests a protective effect of green tea against hematologic neoplasms, especially acute myeloid leukemias.

read more

PMID: 

Mol Biol Rep. 2019 Jul 26. Epub 2019 Jul 26. PMID: 31350662

Abstract Title: 

Epigallocatechin gallate attenuates arsenic induced genotoxicity via regulation of oxidative stress in balb/C mice.

Abstract: 

Arsenic is well known genotoxicant which causes the excessive generation of reactive oxygen species (ROS) and inhibition of antioxidant enzyme systems leading to cell damage through the activation of oxidative sensitive signaling pathways. Epigallocatechin gallate (EGCG), the main and active polyphenolic catechin present in green tea, has shown potent antioxidant, free radical scavenging and genoprotective activity in vivo. The present study attempted to investigate antioxidant and geno-protective efficacy of EGCG by regulating arsenic induced oxidative stress in mice. Animals received prophylactic and therapeutic treatments at two different doses (25 and 50 mg/kg b.wt.) of EGCG orally for 15 days and administered arsenic intraperitoneally at dose of 1.5 mg/kg b.wt (1/10th of LD) for 10 days. Arsenic intoxication revealed enhanced ROS production (114%) in lymphocytes; elevated levels of LPO (2-4 fold); reduced levels of hepato-renal antioxidants (approx. 45%) and augmented genomic fragmentation in hepato-renal tissues; increased chromosomal anomalies (78%) and micronucleation (21.93%) in bone marrow cells and comet tailing (25%) in lymphocytes of mice. Both pre and post treatments of EGCG decreased ROS production, restored lipid peroxidation (LPO) and reduced hepato-renal antioxidants levels, reduced the DNA fragmentation, number of chromosomal aberrations (CA), micronucleation (MN), and comet tailing but prophylactic treatment of 50 mg/kg b.wt was the most effective treatment in regulating arsenic induced oxidative stress. The effectiveness of this dose was furthermore validated by calculating the inhibitory index. Thus, results of present work empirically demonstrate free radical scavenging, anti-oxidative and genoprotective efficacy of EGCG against arsenic toxicity.

read more

PMID: 

Nutrients. 2019 Jul 29 ;11(8). Epub 2019 Jul 29. PMID: 31362373

Abstract Title: 

Low dose Epigallocatechin Gallate Alleviates Experimental Colitis by Subduing Inflammatory Cells and Cytokines, and Improving Intestinal Permeability.

Abstract: 

BACKGROUND: In this study, we investigate the impact of epigallocatechin gallate (EGCG), the most abundant and potent catechin in green tea, on a mouse model of inflammatory bowel disease (IBD) and the underlying mechanisms of action.METHODS: C57BL/6J mice were subjected to dextran sulfate sodium (DSS)-induced IBD-like disease and then randomly divided into three groups: Model group (MD), low-dose EGCG group (LE, 20 mg/kg/d), and high-dose EGCG group (HE, 50 mg/kg/d). DSS-induced clinical and macroscopic changes were monitored daily. Intestinal permeability was assessed by FITC-Dextran assay.RESULTS: Both high- and low-dose EGCG treatment alleviated clinical manifestations including body weight loss and disease activity index (DAI) of DSS-induced colitis. The DAI score was significantly improved after two days of EGCG treatment. At the end of the study, the macroscopic severity score (MSS) of HE and LE treatment groups were 2.4± 1.2, and 2.2 ± 1.0, respectively, significantly lower than that of the controls (5.0 ± 2.1). EGCG treatment also prevented colon shortening, and improved intestinal permeability and histopathological changes. In addition, EGCG treatment attenuated colon inflammation by suppressing colonic levels of pro-inflammatory cytokines IL-6, MCP-1, and TNF-alpha, and inhibited CD3+ T cell and CD68+ macrophage infiltration.CONCLUSION: EGCG is effective in inflammatory colitis because it reduces cellular and molecular inflammation, and reduces intestinal permeability.

read more