PMID: 

Food Funct. 2019 Sep 1 ;10(9):6147-6156. Epub 2019 Sep 9. PMID: 31498347

Abstract Title: 

The synergistic effect of Lactobacillus plantarum CCFM242 and zinc on ulcerative colitis through modulating intestinal homeostasis.

Abstract: 

The beneficial effects of the essential metal zinc (Zn) and probiotics on gut health have been well documented, but how they synergistically affect intestinal physiology is not thoroughly understood. In this study, the Zn-enriching ability of 33 probiotics in a medium or an aqueous solution was evaluated. A Lactobacillus plantarum strain, CCFM242, with a superior Zn-enriching ability was screened. Among the cellular components, the cell wall played the most important role in the Zn binding of L. plantarum CCFM242. The carboxyl and amino groups on the surface of the strain were also vital for Zn enrichment. Upon optimization of the Zn-enriching procedure, the Zn-binding ability of this strain reached 24.89± 0.50 mg gdry biomass. Compared to the treatment of ZnSOor L. plantarum CCFM242, oral supplementation with Zn-enriched L. plantarum CCFM242 resulted in a higher serum Zn level, enhanced levels of mRNA expression of colonic tight junctions, increased levels of short-chain fatty acids (SCFAs) in colonic contents, and stronger modulatory effects on the anti-oxidant and immune defense systems in the gut of normal mice. Zn-Enriched L. plantarum CCFM242 treatment also offered more significant protective effects against dextran sodium sulfate (DSS)-induced colitis in mice compared to the treatment of ZnSOor L. plantarum CCFM242 alone. The synergistic effect of Zn-enriched L. plantarum CCFM242 may be due to the increased tolerance of the strain to the gastrointestinal tract conditions and the higher bioavailability of Zn after the metal-enrichment process.

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PMID: 

Appl Microbiol Biotechnol. 2019 Sep 12. Epub 2019 Sep 12. PMID: 31515596

Abstract Title: 

Protective effects of Lactobacillus plantarum against chronic alcohol-induced liver injury in the murine model.

Abstract: 

Long-term alcohol consumption causes liver injuries such as alcoholic hepatitis, fatty liver, and endotoxemia. Some probiotics were demonstrated to exert beneficial effects in the gastrointestinal tract. The present study was aimed to evaluate the protective effects of Lactobacillus plantarum CMU995 against alcohol-induced liver injury. The mice were orally administered L. plantarum CMU995 for 1 week, followed by the administration of alcohol and different tested substances daily for 6 weeks. The liver injury was examined by measuring the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), malondialdehyde (MDA), anti-oxidative enzyme, endotoxin, inflammatory cytokines, and lipid accumulation in the liver or serum among different groups. L. plantarum CMU995 exhibited beneficial effects on alcohol-induced liver injury via reduction in the serum concentration of AST, ALT, cholesterol, triglycerides, endotoxin, TNF-α, IL-1β, and oxidative stress. Furthermore,we also found that the levels of glutathione (GSH), superoxide dismutase (SOD), and intestinal tight junction protein zonula occludens-1 (ZO-1) were considerably higher in L. plantarum CMU995-fed groups when compared with placebo group. Meanwhile, the protective effects were demonstrated biologicalgradients as controversial dose-dependent. We speculate that L. plantarum CMU995 inhibited the migration of alcohol-derived endotoxin into the blood and liver, thereby improving the intestinal barrier. The present evidence may provide a novel microbiota-based strategy to prevent the alcohol-inducedliver injury.

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PMID: 

Arch Med Sci. 2019 Sep ;15(5):1336-1344. Epub 2019 Jul 12. PMID: 31572482

Abstract Title: 

Effect ofN1115 and fructooligosaccharides in nonalcoholic fatty liver disease.

Abstract: 

Introduction: Nonalcoholic fatty liver disease (NAFLD) is a growing health concern worldwide. Administration of probiotics and prebiotics has been proposed as a convenient and effective treatment. Our study aims to evaluate the therapeutic benefits ofN1115 (N1115) and fructooligosaccharides (FOS) by examining the histopathogenesis and underlying molecular events of NAFLD.Material and methods: An NAFLD mouse model was established by feeding C57BL/6 mice with a high-fat diet (HFD). N1115, FOS and synbiotics were administered for 16 weeks.Results: N1115, FOS and synbiotics alleviated HFD-induced hepatic steato-sis and release of tumor necrosis factor-α, and slowed the progression of cirrhosis. Compared to the HFD group, these dietary supplements reduced serum total triglyceride and cholesterol, and appeared to decrease the fasting blood glucose and insulin. Intraperitoneal glucose tolerance tests, homeostatic model assessment of insulin resistance and real-time PCR showed that the regimens could overcome insulin resistance. These findings were associated with the transcriptional repression of inflammatory factors such as lipopolysaccharides, Toll-like receptor 4 and nuclear factor-κB. Lastly, N1115, FOS, and synbiotics improved the intestinal barrier functions and histologic integrity. This was accompanied by the restoration of the p38 MAPK pathway and in-creased expression of the tight junction components occludin-1 and claudin-1.Conclusions: N1115, FOS and synbiotics are effective in the prevention and treatment of NAFLD. Our data support the translation of these agents into clinical evaluation in human subjects with NAFLD and/or associated risk factors.

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PMID: 

J Microbiol Biotechnol. 2019 Sep 9. Epub 2019 Sep 9. PMID: 31546298

Abstract Title: 

Oral Administration ofβ-Glucan andAlleviates Atopic Dermatitis-like Symptoms.

Abstract: 

Atopic dermatitis (AD) is a chronic inflammatory skin disease of mainly infants and children. Currently, the development of safe and effective treatments for AD is urgently required. The present study was conducted to investigate the immunomodulatory effects of yeast-extractedβ-1,3/1,6-glucan and/or() LM1004 against AD-like symptoms. To purpose,β-1,3/1,6-glucan and/orLM1004 were orally administered to AD-induced animal models of rat (histamine-induced vasodilation) and mouse (pruritus and contact dermatitis) exhibiting different symptoms of AD. We then investigated the treatment effects on AD-like symptoms, gene expression of immune-related factors, and gut microbiomes. Oral administration ofβ-1,3/1,6-glucan (0.01g/kg initial body weight) and/or 2×10cells/gLM1004 (0.01g/kg initial body weight) to AD-induced animal models showed significantly reduced vasodilation in the rat model, and pruritus, edema, and serum histamine in the mouse models (

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PMID: 

Wien Klin Wochenschr. 2011 Jan ;123(1-2):38-40. Epub 2011 Jan 19. PMID: 21240685

Abstract Title: 

Citric acid inhibits growth of Helicobacter pylori in vitro: a new strategy for eradication.

Abstract: 

BACKGROUND: About 50% of the world population is infected with Helicobacter pylori. The association of peptic ulcer disease with Helicobacter pylori is well documented. Therefore eradication is obligatory. However, the high costs of multidrug therapy, the resistance of Helicobacter pylori to antibiotics as well as the sometimes present drug intolerance are limiting factors.METHODS: The inhibitory effect of 3% hydrogen peroxide, 8.4% sodium bicarbonate, 2% ascorbic acid, citric acid in combination with sodium citrate, 7% and 14% citric acid solutions, respectively, on nine Helicobacter pylori strains were tested in vitro.RESULTS: Citric acid showed a potent inhibitory activity on growth of Helicobacter pylori strains in vitro. This was observed not only when citric acid was applied alone but also if citric acid was given together with low concentration of sodium citrate. Two percent ascorbic acid inhibited three, sodium bicarbonate two and hydrogen peroxide one of the nine tested Helicobacter pylori strains, respectively.CONCLUSIONS: Citric acid is a cheap substance present in many fruits and produced by food industry, and it demonstrated powerful inhibitory effect on the growth of Helicobacter pylori strains. On the basis of our findings citric acid should be further evaluated for the eradication of Helicobacter pylori.

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PMID: 

Biochem Biophys Res Commun. 2010 Feb 26 ;393(1):118-22. Epub 2010 Feb 1. PMID: 20117096

Abstract Title: 

Citric acid inhibits development of cataracts, proteinuria and ketosis in streptozotocin (type 1) diabetic rats.

Abstract: 

Although many fruits such as lemon and orange contain citric acid, little is known about beneficial effects of citric acid on health. Here we measured the effect of citric acid on the pathogenesis of diabetic complications in streptozotocin-induced diabetic rats. Although oral administration of citric acid to diabetic rats did not affect blood glucose concentration, it delayed the development of cataracts, inhibited accumulation of advanced glycation end-products (AGEs) such as N(epsilon)-(carboxyethyl)lysine (CEL) and N(epsilon)-(carboxymethyl)lysine (CML) in lens proteins, and protected against albuminuria and ketosis. We also show that incubation of protein with acetol, a metabolite formed from acetone by acetone monooxygenase, generate CEL, suggesting that inhibition of ketosis by citric acid may lead to the decrease in CEL in lens proteins. These results demonstrate that the oral administration of citric acid ameliorates ketosis and protects against the development of diabetic complications in an animal model of type 1 diabetes.

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PMID: 

J Tissue Viability. 2014 Feb ;23(1):24-8. Epub 2013 Dec 28. PMID: 24411100

Abstract Title: 

Citric acid treatment of post operative wound infections in HIV/AIDS patients.

Abstract: 

The normal cellular immunity is required for normal wound healing. The HIV infection affects wound healing adversely. Wound infections in HIV/AIDS patients are difficult to manage because of compromised immunity. The result is delayed wound healing and increased susceptibility to wound infection. Here we report two cases of HIV positive patients who had developed the post operative wound gape, not responding to the conventional treatment, treated simply by local application of three percent citric acid ointment.

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Our modern world is a difficult place to maintain a healthful balance. Ginger is, hands down, one of the most broadly therapeutic and familiar plant allies available to us to prevent and even reverse a wide range of ailments, with the science supporting its safety and efficacy one of the most robust. 

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PMID: 

J Appl Physiol (1985). 2019 Jul 25. Epub 2019 Jul 25. PMID: 31343948

Abstract Title: 

Beet the cold: Beetroot juice improves peripheral blood flow, endothelial function and anti-inflammatory status in individuals with Raynaud's phenomenon.

Abstract: 

Raynaud's phenomenon (RP) is characterised by recurrent transient peripheral vasospasm and lower nitric oxide (NO) bioavailability in the cold. We investigated the effect of nitrate-rich beetroot juice (BJ) supplementation onNO-mediated vasodilation,cutaneous vascular conductance (CVC) and skin temperature (T) following local cooling andsystemic anti-inflammatory status. Following baseline testing, twenty-three individuals with RP attended four times, in a double-blind, randomized crossover design, following acute and chronic (14 days) BJ and nitrate-depleted beetroot juice (NDBJ) supplementation. Peripheral Tand CVC were measured during and after mild hand and foot cooling, and during transdermal delivery of acetylcholine and sodium nitroprusside. Markers of anti-inflammatory status were also measured. Plasma [nitrite] was increased in the BJ conditions (0.05). Plasma [interleukin-10] was greater, pan endothelin and systolic and diastolic blood pressure (BP) were reduced, and forearm endothelial function was improved ,by both BR and NDBJ supplementation (

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PMID: 

Biomolecules. 2019 Jul 7 ;9(7). Epub 2019 Jul 7. PMID: 31284640

Abstract Title: 

Ameliorative Effect ofRoot Extract on Chlorpyrifos-Induced Oxidative Stress, Inflammation and Liver Injury in Rats.

Abstract: 

Exposure to organophosphorus insecticides causes several health problems to animals and humans. Red beetroot (RBR) is rich in antioxidant ingredients and possesses a promising hepatoprotective activity. This study evaluated the potential of RBR extract to prevent chlorpyrifos (CPF)-induced liver injury, with an emphasis on oxidative stress, inflammation and apoptosis. Rats received 10 mg/kg CPF and were treated with 300 mg/kg RBR extract for 28 days. CPF caused liver injury evidenced by elevated serum levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and bilirubin, along with several histological alterations. Hepatic lipid peroxidation (LPO) and nitric oxide (NO) levels, as well as inducible nitric oxide synthase (iNOS) and pro-inflammatory cytokines were increased in CPF-intoxicated rats. RBR prevented CPF-induced histological alterations, and ameliorated liver function, LPO, NO, iNOS and pro-inflammatory cytokines. RBR boosted glutathione and antioxidant enzymes, and increased Nrf2 expression. In addition, RBR diminished Bax and caspase-3, and increased Bcl-2 expression. In conclusion, RBR prevented CPF-induced liver injury via attenuation of oxidative stress, inflammation and apoptosis. RBR enhanced antioxidant defenses, suggesting that it could be used as a potential therapeutic intervention to minimize CPF hepatotoxicity.

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