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EGCG was able to exert anti-benign prostatic hyperplasia activities in metabolic syndrome rats.6/29/2016
PMID: Environ Toxicol Pharmacol. 2016 Jun 15 ;45:315-320. Epub 2016 Jun 15. PMID: 27348728 Abstract Title: Protective potential of epigallocatechin-3-gallate against benign prostatic hyperplasia in metabolic syndrome rats. Abstract: Epigallocatechin-3-gallate (EGCG) is a major catechin in green tea with functions of antioxidant, anti-proliferative, anti-inflammatory and attenuating metabolic syndrome. In this study, rat model of benign prostatic hyperplasia (BPH) accompanied with metabolic syndrome was induced by fed on high-fat diet for 12 weeks combined with testosterone injection (10mg/kg/d) from 9th to 12th weeks. EGCG was orally given from 9th to 12th weeks. Finally, the levels of glucose, total cholesterol, triglyceride, prostate weight, insulin-like growth factors (IGFs), inflammatory cytokines, antioxidant enzymes, and prostatic expression of IGF binding protein-3 (IGFBP-3) and peroxisome proliferator activated receptors (PPARs) were evaluated. It was found that EGCG significantly decreased the levels of glucose, total cholesterol, triglyceride, IGFs, and inflammatory cytokines, normalized the activities of antioxidant enzymes, as well as increased the prostatic expression of IGFBP-3 and PPARs. These results indicated that EGCG was able to exert anti-BPH activities in metabolic syndrome rats.
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PMID: Med Sci Monit. 2016 ;22:2152-60. Epub 2016 Jun 23. PMID: 27333866 Abstract Title: Astaxanthin Inhibits Proliferation and Induces Apoptosis and Cell Cycle Arrest of Mice H22 Hepatoma Cells. Abstract: BACKGROUND It is widely recognized that astaxanthin (ASX), a member of the carotenoid family, has strong biological activities including antioxidant, anti-inflammation, and immune-modulation activities. Previous studies have confirmed that ASX can effectively inhibit hepatoma cells in vitro. MATERIAL AND METHODS MTT was used to assay proliferation of mice H22 cells, and flow cytometry was used to determine apoptosis and cell cycle arrest of H22 cells in vitro and in vivo. Moreover, anti-tumor activity of ASX was observed in mice. RESULTS ASX inhibited the proliferation of H22 cells, promoted cell necrosis, and induced cell cycle arrest in G2 phase in vitro and in vivo. CONCLUSIONS This study indicated that ASX can inhibit proliferation and induce apoptosis and cell cycle arrest in mice H22 hepatoma cells in vitro and in vivo.
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PMID: J Oral Pathol Med. 2016 Jun 17. Epub 2016 Jun 17. PMID: 27314762 Abstract Title: Evaluation of efficacy of aloe vera in the treatment of oral submucous fibrosis - a clinical study. Abstract: BACKGROUND: Oral submucous fibrosis is a chronic disease, treatment of which has largely been symptomatic. Aloe vera has immunomodulatory, anti-inflammatory, wound healing, antioxidant, and antineoplastic activities. All such properties of aloe vera suggest the possibility of its use in the management of oral submucous fibrosis.METHODS: Seventy-four patients of oral submucous fibrosis were randomly divided into 2 groups. Group A patients were treated with systemic (juice) and topical aloe vera (gel) for 3 months. Group B patients were treated with intralesional injection of hydrocortisone and hyaluronidase for 6 weeks with antioxidant supplements for 3 months. Patients were assessed for reduction in burning sensation and increase in mouth opening, cheek flexibility, and tongue protrusion at an interval of 1, 2, and 3 months.RESULTS: Both the groups showed statistically significant improvements in all the study parameters at the end of study period (P
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PMID: Oncotarget. 2016 Jun 15. Epub 2016 Jun 15. PMID: 27323816 Abstract Title: Could gut microbiota serve as prognostic biomarker associated with colorectal cancer patients' survival? A pilot study on relevant mechanism. Abstract: Evidences have shown that dysbiosis could promote the progression of colorectal cancer (CRC). However, the association of dysbiosis and prognosis of CRC is barely investigated. Therefore, we used 16S rRNA gene sequencing approach to determine differences in microbiota among tumor tissues of different prognosis and found that Fusobacterium nucleatum and Bacteroides fragilis were more abundant in worse prognosis groups, while Faecalibacterium prausnitzii displayed higher abundance in survival group. To further explore the prognostic value of the found bacteria, Kaplan-Meier and Cox proportional regression analyses were used and the results exhibited that high abundance of F. nucleatum and B. fragilis were independent indicators of poor patient's survival. Besides, the expression of major inflammatory mediator were analyzed using PCR and western blot methods, and it turned out that high abundance of F. nucleatum was associated with increased expression of TNF-α, β-catenin and NF-κB, while COX-2, MMP-9 and NF-κB were positively related with high B. fragilis level, and high level of F. prausnitzii showed lower expression of β-catenin, MMP-9 and NF-κB. Moreover, immunohistochemical analysis indicated that KRAS and BRAF expression were prominent in F.nucleatum and B. fragilis high abundance group, while MLH1 showed lower expression. In conclusion, F. nucleatum, B. fragilis and F. prausnitzii can be identified as useful prognostic biomarkers for CRC, and dysbiosis might worsen the patients' prognosis by up-regulating gut inflammation level.
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PMID: Alzheimers Dement (Amst). 2016 ;2:49-57. Epub 2016 Feb 4. PMID: 27239536 Abstract Title: Periodontal disease's contribution to Alzheimer's disease progression in Down syndrome. Abstract: People with Down syndrome (DS) are at an increased risk for Alzheimer's disease (AD). After 60 years of age,>50% of DS subjects acquire dementia. Nevertheless, the age of onset is highly variable possibly because of both genetic and environmental factors. Genetics cannot be modified, but environmental risk factors present a potentially relevant intervention for DS persons at risk for AD. Among them, inflammation, important in AD of DS type, is potential target. Consistent with this hypothesis, chronic peripheral inflammation and infections may contribute to AD pathogenesis in DS. People with DS have an aggressive form of periodontitis characterized by rapid progression, significant bacterial and inflammatory burden, and an onset as early as 6 years of age. This review offers a hypothetical mechanistic link between periodontitis and AD in the DS population. Because periodontitis is a treatable condition, it may be a readily modifiable risk factor for AD.
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PMID: Nat Rev Gastroenterol Hepatol. 2016 Jul ;13(7):412-25. Epub 2016 Jun 8. PMID: 27273168 Abstract Title: The role of the gut microbiota in NAFLD. Abstract: NAFLD is now the most common cause of liver disease in Western countries. This Review explores the links between NAFLD, the metabolic syndrome, dysbiosis, poor diet and gut health. Animal studies in which the gut microbiota are manipulated, and observational studies in patients with NAFLD, have provided considerable evidence that dysbiosis contributes to the pathogenesis of NAFLD. Dysbiosis increases gut permeability to bacterial products and increases hepatic exposure to injurious substances that increase hepatic inflammation and fibrosis. Dysbiosis, combined with poor diet, also changes luminal metabolism of food substrates, such as increased production of certain short-chain fatty acids and alcohol, and depletion of choline. Changes to the microbiome can also cause dysmotility, gut inflammation and other immunological changes in the gut that might contribute to liver injury. Evidence also suggests that certain food components and lifestyle factors, which are known to influence the severity of NAFLD, do so at least in part by changing the gut microbiota. Improved methods of analysis of the gut microbiome, and greater understanding of interactions between dysbiosis, diet, environmental factors and their effects on the gut-liver axis should improve the treatment of this common liver disease and its associated disorders.
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PMID: Arthritis Rheumatol. 2016 Jun 22. Epub 2016 Jun 22. PMID: 27333153 Abstract Title: Dysbiosis contributes to arthritis development via activation of autoreactive T cells in the intestine. Abstract: OBJECTIVE: The intestinal microbiota is involved in arthritis pathogenesis. Altered microbiota composition has been demonstrated in rheumatoid arthritis (RA) patients. However, it remains unclear how dysbiosis contributes to arthritis development. We investigated whether the altered composition of human intestinal microbiota in RA patients contributes to the development of arthritis.METHODS: We analyzed fecal microbiota of early RA patients and healthy controls by 16S rRNA-based deep sequencing. We inoculated fecal samples from RA patients and healthy controls into germ-free arthritis-prone SKG mice and evaluated immune responses. We also analyzed whether lymphocytes of SKG mice harboring microbiota from RA patients react with arthritis-related autoantigen, RPL23A.RESULTS: A subpopulation of early RA patients harbored intestinal microbiota dominated by Prevotella copri; SKG mice harboring microbiota from RA patients contained an increased number of intestinal Th17 cells and developed severe arthritis upon zymosan treatment. Lymphocytes in regional lymph nodes and colon, but not spleen, of these mice showed enhanced IL-17 responses to RPL23A. Naïve SKG T cells, co-cultured with P. copri-stimulated dendritic cells, produced IL-17 in response to RPL23A and rapidly induced arthritis.CONCLUSIONS: We showed that dysbiosis increases the sensitivity to arthritis via activation of autoreactive T cells in the intestine. Autoreactive SKG T cells are activated by dysbiotic microbiota in the intestine, causing joint inflammation. Dysbiosis is an environmental factor that triggers arthritis development in genetically susceptible mice. This article is protected by copyright. All rights reserved.
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PMID: World J Clin Oncol. 2014 Aug 10 ;5(3):455-64. PMID: 25114859 Abstract Title: Modification in the diet can induce beneficial effects against breast cancer. Abstract: The population tends to consume foods that in addition to their nutritional values can offer some benefits to their health. There are many epidemiological evidences and research studies in animal models suggesting that diet plays an important role in breast cancer prevention or progression. This review summarized some of the relevant researches about nutrition and cancer during the last years, especially in breast cancer. The analysis of probiotics and fermented products containing lactic acid bacteria in cancer prevention and/or treatment was especially discussed. It was observed that a balance of fatty acids similar to those of traditional Mediterranean diet, the consumption of fruits and vegetables, dietary fiber intake, vitamin supplementation are, along with the intake of probiotic products, the most extensively studied by the negative association to breast cancer risk. The consumption of probiotics and fermented products containing lactic acid bacteria was associated to reduce breast cancer risk in some epidemiological studies. The use of animal models showed the modulation of the host's immune response as one of the important effects associated to the benefices observed with most probiotics. However; future assays in human are very important before the medical community can accept the addition of probiotic or fermented milks containing lactic acid bacteria as supplements for cancer patients.
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PMID: PLoS One. 2014 ;9(1):e83744. Epub 2014 Jan 8. PMID: 24421902 Abstract Title: Microbial dysbiosis is associated with human breast cancer. Abstract: Breast cancer affects one in eight women in their lifetime. Though diet, age and genetic predisposition are established risk factors, the majority of breast cancers have unknown etiology. The human microbiota refers to the collection of microbes inhabiting the human body. Imbalance in microbial communities, or microbial dysbiosis, has been implicated in various human diseases including obesity, diabetes, and colon cancer. Therefore, we investigated the potential role of microbiota in breast cancer by next-generation sequencing using breast tumor tissue and paired normal adjacent tissue from the same patient. In a qualitative survey of the breast microbiota DNA, we found that the bacterium Methylobacterium radiotolerans is relatively enriched in tumor tissue, while the bacterium Sphingomonas yanoikuyae is relatively enriched in paired normal tissue. The relative abundances of these two bacterial species were inversely correlated in paired normal breast tissue but not in tumor tissue, indicating that dysbiosis is associated with breast cancer. Furthermore, the total bacterial DNA load was reduced in tumor versus paired normal and healthy breast tissue as determined by quantitative PCR. Interestingly, bacterial DNA load correlated inversely with advanced disease, a finding that could have broad implications in diagnosis and staging of breast cancer. Lastly, we observed lower basal levels of antibacterial response gene expression in tumor versus healthy breast tissue. Taken together, these data indicate that microbial DNA is present in the breast and that bacteria or their components may influence the local immune microenvironment. Our findings suggest a previously unrecognized link between dysbiosis and breast cancer which has potential diagnostic and therapeutic implications.
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PMID: Medicine (Baltimore). 2016 Feb ;95(6):e2584. PMID: 26871778 Abstract Title: The Efficacy of Ginseng-Related Therapies in Type 2 Diabetes Mellitus: An Updated Systematic Review and Meta-analysis. Abstract: Few randomized clinical trials have evaluated the efficacy of ginseng in patients with type 2 diabetes mellitus (T2DM). The current meta-analysis evaluated the ginseng-induced improvement in glucose control and insulin sensitivity in patients with type-2 diabetes or impaired glucose tolerance.Randomized clinical trials comparing ginseng supplementation versus control, in patients with T2DM or impaired glucose tolerance, were hand-searched from Medline, Cochrane, and Google Scholar databases by 2 independent reviewers using the terms"type 2 diabetes/diabetes/diabetic, impaired glucose tolerance, and ginseng/ginsenoside(s)."The primary outcome analyzed was the change in HbA1c, whereas the secondary outcomes included fasting glucose, postprandial glucose, fasting insulin, postprandial insulin, insulin resistance Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), triglycerides, total cholesterol, low density lipoprotein (LDL), and high density lipoprotein (HDL).Of the 141 studies identified, 8 studies were chosen for the current meta-analysis. The average number of patients, age, and sex distribution among the groups were comparable. Results reveal no significant difference in HbA1c levels between the ginseng supplementation and the control groups (pooled standardized difference in means = -0.148, 95% CI: -0.637 to 0.228, P = 0.355). Ginseng supplementation improved fasting glucose, postprandial insulin, and HOMA-IR levels, though no difference in postprandial glucose or fasting insulin was observed among the groups. Similarly, triglycerides, total cholesterol, and LDL levels showed significant difference between the treatment groups, while no difference in HDL was seen. In addition, ginseng-related therapy was ineffective in decreasing the fasting glucose levels in patients treated with oral hypoglycemic agents or insulin.The present results establish the benefit ofginseng supplementation in improving glucose control and insulin sensitivity in patients with T2DM or impaired glucose intolerance.
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