Selenium modulated gut flora and promoted decomposition of methylmercury in methylmercury-poisoned rats.

PMID: 

Ecotoxicol Environ Saf. 2019 Dec 15 ;185:109720. Epub 2019 Oct 1. PMID: 31585392

Abstract Title: 

Selenium modulated gut flora and promoted decomposition of methylmercury in methylmercury-poisoned rats.

Abstract: 

INTRODUCTION: Selenium plays important roles in antagonizing the toxicity of methylmercury. The underlying mechanism for the antagonism between Se and MeHg is still not fully understood.OBJECTIVE: The role of gut flora against the toxicity of environmental contaminants is receiving more and more attention. The objective of this study was to investigate the role of Se against MeHg-poisoning in the modulation of gut flora and the decomposition of MeHg.METHODS: MeHg-poisoned rats were treated with sodium selenite every other day for 90 days. Fecal samples were collected on Day 8, 30, 60 and 90. Gut flora in feces was determined using 16S rRNA gene profiling, and the concentrations of Se and total mercury (THg) were measured by ICP-MS, and the concentration of MeHg was measured by CVAFS.RESULTS: Gut flora at both the ranks of phylum and genus in the MeHg-poisoned rats after Se treatment was modulated towards that in the control group, suggesting the restoration of the profile of gut flora. Increased THg was found in fecal samples after Se treatment on day 30. The percentage of MeHg (of total mercury) in the MeHg-poisoned group was in the range of 81-105% while it was 65-84% in the Se treatment group on different days, suggesting the increased decomposition of MeHg in MeHg-poisoned rats after Se treatment.CONCLUSIONS: This study suggests that MeHg poisoning damaged the abundance of gut flora and decreased their capacity for the decomposition of MeHg. After Se treatment, the abundance of gut flora was partially restored and the decomposition and excretion of MeHg was enhanced. These findings suggest that the modulation of gut flora may be one way to promote the health status in MeHg-poisoned rats and possibly in human beings.

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Sesamin exerts anti-aging effects in the muscles, brain and midgut by inducing antioxidative and DNA repair genes.

PMID: 

Eur Rev Med Pharmacol Sci. 2019 Feb ;23(4):1826-1839. PMID: 30840309

Abstract Title: 

Sesamin suppresses aging phenotypes in adult muscular and nervous systems and intestines in a Drosophila senescence-accelerated model.

Abstract: 

OBJECTIVE: Sesamin is a major lignan constituent of sesame and possesses various health-promoting effects. Previous studies have demonstrated that sesamin extends the lifespan of Drosophila and Caenorhabditis elegans and corrects oxidative damage-related tissue dysfunction in mammals. To understand its anti-agingeffects, we aimed to determine whether sesamin restores tissue function hampered by oxidative damage and suppresses several aging-related phenotypes using Drosophila senescence-accelerated models.MATERIALS AND METHODS: We elucidated the anti-aging effects of sesamin on several aging-related phenotypes in the muscle, brain and midgut using the senescence-accelerated models (Sod1n1 mutant and Sod1-depleted flies) by immunostaining experiments. We determined the expression levels of several anti-oxidative and DNA repair genes using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). We also identified the metabolite of sesamin in Drosophila by LC-MS/MS.RESULTS: We confirmed that sesamin (0.35 and 2 mg/ml) extended the lifespan of the fly models. As observed in mammals, it can be absorbed and metabolized by Drosophila adults. The sesamin feeding suppressed the age-dependent impairment of locomotor activity and inhibited the accumulation of reactive oxygen species (ROS) in their bodies. Sesamin delayed the age-dependent accumulation of damaged proteins in the muscle, partially suppressed the loss of dopaminergic neurons in adult brains displaying ROS accumulation, and suppressed the accumulation of DNA damage and hyperproliferation of intestinal stem cells. Four antioxidative genes and two DNA repair genes were simultaneously upregulated in sesamin-fed adults. CONCLUSIONS: These observations represent the first direct evidence of the anti-aging effects of sesamin at the individual level. We propose that sesamin exerts anti-aging effects in the muscles, brain and midgut by inducing antioxidative and DNA repair genes, resulting in extended lifespan in flies.

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Welcome 5G Crisis Summit Supporters! 

GreenMedInfo.com contains research on over 10,000 different health related topics. The one featured for the 5G and EMF advocacy communities is called “Electromagnetic Fields,” and contains hundreds of abstracts on signals of harm associated with these anthropogenic radiofrequencies related to 30+ different diseases. View the research here: Electromagnetic Fields.

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Sesamin could be a promising potential therapeutic agent against diabetes-associated cognitive decline.

PMID: 

Life Sci. 2019 Aug 1 ;230:169-177. Epub 2019 May 29. PMID: 31150685

Abstract Title: 

Sesamin: A promising protective agent against diabetes-associated cognitive decline in rats.

Abstract: 

AIMS: Hippocampal oxidative stress and apoptosis of CA1 neurons play significant roles in the pathophysiology of diabetes-associated cognitive decline (DACD). The present study was aimed to elucidate the putative effects of sesamin, a major lignan of sesame seed, against DACD, and possible involvement of anti-oxidative and anti-apoptotic mechanisms.MAIN METHODS: Fifty adult male Wistar rats were randomly divided into control, control-sesamin (30 mg/kg/day), diabetic, diabetic-sesamin (30 mg/kg/day), and diabetic-insulin (6 IU/rat/day) groups. Diabetic rats were treated with sesamin (P.O.) or insulin (S.C.) for eight consecutive weeks. Cognitive performance was evaluated in a Morris Water Maze (MWM) test; in addition, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and malondialdehyde (MDA) concentrations were assayed in the hippocampus using assay kits. Moreover, hematoxylin-eosin (HE), TUNEL, and immunohistochemistry (IHC) stainings were conducted to evaluate histological changes, the apoptosis statusand expression of pro- and anti-apoptotic proteins in the hippocampal CA1 neurons, respectively.KEY FINDINGS: The results showed that diabetes reduced the spatial cognitive ability in MWM, which was accompanied by decrease in SOD, CAT, and GPx activities and increase in MDA level in the hippocampus. Additionally, diabetes resulted in neuronal loss, enhanced apoptotic index, elevated the expression of pro-apoptotic Bax protein, and decreased the expression of anti-apoptotic Bcl-2 protein in the hippocampal CA1 neurons. Interestingly, sesamin treatment improved all the above-mentioned deficits of diabetes at a comparable level with insulin therapy.SIGNIFICANCE: The results suggest that sesamin could be a promising potential therapeutic agent against DACD, possibly through its intertwined anti-hyperglycemic, anti-oxidative, and anti-apoptotic properties.

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Sesamin promotes osteoblastic differentiation and protects rats from osteoporosis.

PMID: 

Med Sci Monit. 2019 Jul 17 ;25:5312-5320. Epub 2019 Jul 17. PMID: 31314750

Abstract Title: 

Sesamin Promotes Osteoblastic Differentiation and Protects Rats from Osteoporosis.

Abstract: 

BACKGROUND Osteoporosis is a common osteopathy, resulting in fractures, especially in elder people. Sesamin has many pharmacological effects, including supplying calcium. However, how sesamin might prevent osteoporosis is still under study. MATERIAL AND METHODS Bone marrow stromal cells (BMSCs) extracted from rat femur were induced for osteoblastic differentiation. Cell proliferation, alkaline phosphatase (ALP), osterix (OSX), SRY-box 9 (SOX9), runt-related transcription factor 2 (RUNX2), osteocalcin (OCN),ß-catenin, low density lipoprotein receptor-related protein 5 (LRP5), and glycogen synthase kinase-3ß (GSK-3ß) levels in BMSCs were detected in the presence or absence of sesamin (1 μM or 10 µM). In addition, FH535 (1 μM) was used to silence Wnt/ß-catenin in vitro. Ovariectomized (OVX) rats were established and intragastrically administrated sesamin (80 mg/kg), and then the rat bones were analyzed by micro-computed tomography. Osteocalcin and collagen type I were measured in the rat femurs. RESULTS Sesamin had no influence on BMSC proliferation. Higher sesamin concentration promoted Wnt/ß-catenin activity and enhanced more expressions of ALP, OSX, SOX9, RUNX2, and OCN, gradually and significantly (P

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Sesamin enhances Nrf2-mediated protective defense against oxidative stress and inflammation in colitis.

PMID: 

Oxid Med Cell Longev. 2019 ;2019:2432416. Epub 2019 Aug 26. PMID: 31534619

Abstract Title: 

Sesamin Enhances Nrf2-Mediated Protective Defense against Oxidative Stress and Inflammation in Colitis via AKT and ERK Activation.

Abstract: 

Ulcerative colitis (UC) is a major form of inflammatory bowel disease (IBD) with high incidence and prevalence in many countries. Patients with UC usually suffer from a lifetime of debilitating physical symptoms. Therefore, developing effective therapeutic strategy that can manage this disease better and improve patients' life quality is in urgent need. Sesamin (SSM) is a lignan derived from sesame seeds. In this study, the protective effect of SSM against UC and the underlying mechanism were investigatedand. Our data showed that SSM protected Caco-2 cells from HO-induced oxidative stress injury via GSH-mediated scavenging of reactive oxygen species (ROS). Dual luciferase reporter assay showed that the transcriptional activity of nuclear factor erythroid-related factor 2 (Nrf2) was significantly increased by SSM, and the ability of SSM to activate Nrf2-targeted genes was further confirmed in Caco-2 cells using western blot and quantitative real-time PCR (qRT-PCR). In contrast, Nrf2 knockdown abolished the protective effect of SSM. Additionally, we found that SSM also activated advanced protein kinase B (AKT) and extracellular signal-regulated kinase (ERK) in Caco-2 cells, while either AKT or ERK inhibition can prevent SSM-mediated nuclear translocation of Nrf2. Furthermore, SSM displayed a better protective effect against dextran sulfate sodium- (DSS-) induced UC compared with 5-aminosalicylic acid (5-ASA) in C57BL/6 mice. The enhanced Nrf2 signaling and activated AKT/ERK were also observed in the colon of mice after SSM administration. These results first demonstrate the protective effect of SSM against UC and indicate that the effect is associated with AKT/ERK activation and subsequent Nrf2 signaling enhancement. This study provides a new insight into the medicinal value of SSM and proposes it as a new natural nutrition for better managing the symptoms of UC.

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Sesamin has potential for use as a skin protection agent in antiphotodamage and skin care products.

PMID: 

Biomolecules. 2019 Sep 12 ;9(9). Epub 2019 Sep 12. PMID: 31547364

Abstract Title: 

Protective Effects of Sesamin against UVB-Induced Skin Inflammation and Photodamage In Vitro and In Vivo.

Abstract: 

Ultraviolet (UV) exposure has been demonstrated as the most critical factor causing extrinsic skin aging and inflammation. This study explored the protective effects and mechanisms of sesamin against skin photodamage. Sesamin reduced intracellular reactive oxygen species production after UVB irradiation in human dermal fibroblasts. The sesamin treatment attenuated mitogen-activated protein (MAP) kinase phosphorylation and matrix metalloproteinase (MMPs) overexpression induced by UVB exposure, and it significantly enhanced the tissue inhibitor of metalloproteinase-1 protein expression. Sesamin also elevated the total collagen content in human fibroblasts by inhibiting UVB-induced mothers against decapentaplegic homolog 7 (Smad7) protein expression. Sesamin reduced UVB-induced inducible nitric oxide synthase (i-NOS) and cyclooxygenase-2 (COX-2) overexpression and inhibited nuclear factor-kappa B (NF-κB) translocation. Moreover, sesamin may regulate the c-Jun N-terminal kinases (JNK) and p38 MAP kinase pathways, which inhibit COX-2 expression. Sesamin could reduce UVB-induced inflammation, epidermal hyperplasia, collagen degradation, and wrinkle formation in hairless mice. It also reduced MMP-1, interleukin (IL-1), i-NOS, and NF-κB in the mouse skin. These results demonstrate that sesamin had antiphotodamage and anti-inflammatory activities. Sesamin has potential for use as a skin protection agent in antiphotodamage and skin care products.

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The protective role of lutein on isoproterenol-induced cardiac failure.

PMID: 

Pharm Biol. 2019 Dec ;57(1):529-535. PMID: 31411934

Abstract Title: 

The protective role of lutein on isoproterenol-induced cardiac failure rat model through improving cardiac morphology, antioxidant status via positively regulating Nrf2/HO-1 signalling pathway.

Abstract: 

Lutein (LU) is a major carotenoid with various pharmacological activities including anti-inflammatory, antioxidant and anti-apoptosis.The cardioprotective efficacy of LU was determined by evaluating the biochemical and histopathological changes in isoproterenol (ISO) induced myocardial infarction (MI) rat model.Healthy male albino rats ( = 40) were segregated into 4 equal groups. Group I (control) rats were administered with olive oil, Group II (LU) rats were orally pre-treated with only 40 mg of LU for 28 days, Group III (MI induced) rats were injected (subcutaneously; s.c) with 85 mg/kg of ISO for 2 consecutive days, whereas Group IV (LU + ISO) rats were pre-treated with 40 mg of LU for 28 days before ISO induction.ISO-induced group showed increased infarct size and cardiac/inflammatory/apoptotic markers. However, pre-treatment with LU (28 days) considerably reduced ( 

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There is ample evidence suggesting that sesamol possesses potent anti-cancer properties in vitro and in vivo.

PMID: 

Eur J Pharmacol. 2019 Jul 15 ;855:75-89. Epub 2019 May 4. PMID: 31063773

Abstract Title: 

Sesamol, a major lignan in sesame seeds (Sesamum indicum): Anti-cancer properties and mechanisms of action.

Abstract: 

Sesamol is a natural phenolic compound and a major lignan isolated from sesame seeds (Sesamum indicum) and sesame oil. The therapeutic potential of sesamol was investigated intensively, and there is compelling evidence that sesamol acts as a metabolic regulator that possesses antioxidant, anti-mutagenic, anti-hepatotoxic, anti-inflammatory, anti-aging, and chemopreventive properties. Various studies have reported that sesamol exerts potent anti-cancer effects. Herein, we provide a comprehensive review that summarizes the in vitro and in vivo anti-cancer activity of sesamol in several cancer cell lines and animal models. The protective role that sesamol plays against oxidative stress through its radical scavenging ability and lipid peroxidation lowering potential is analyzed. The ability of sesamol to regulate apoptosis and various stages of the cell cycle is also outlined. Moreover, the signaling pathways that sesamol seems to target to execute its antioxidant, anti-inflammatory, and pro-apoptotic/anti-proliferative roles are discussed. The signaling pathways that sesamol targets include the p53, MAPK, JNK, PI3K/AKT, TNFα, NF-κB, PPARγ, caspase-3, Nrf2, eNOS, and LOX pathways. The mechanisms of action that sesamol executes to deliver its anti-cancer effects are delineated. In sum, there is ample evidence suggesting that sesamol possesses potent anti-cancer properties in vitro and in vivo. A thorough understanding of the molecular targets of sesamol and the mechanisms of action underlying its anti-cancer effects is necessary for possible employment of sesamol as a chemotherapeutic agent in cancer prevention and therapy.

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Coenzyme Q10 supplementation in fibrosis and aging.

PMID: 

Adv Exp Med Biol. 2019 ;1178:103-112. PMID: 31493224

Abstract Title: 

Coenzyme Q10 Supplementation in Fibrosis and Aging.

Abstract: 

Coenzyme Q10 (CoQ10) is a vitamin-like substance which functions as an electron carrier within the mitochondrial respiratory chain, as well as serving as an important intracellular antioxidant. Most of the body's CoQ10 requirements are met by endogenous synthesis, although the capacity for CoQ10 production decreases substantially with increasing age. In this article we have reviewed the potential role of CoQ10 supplementation in the treatment of tissue fibrosis, which has been implicated in the age-related loss of function of various organs including the heart. Clinical studies have indicated that CoQ10 supplementation may decrease the level of cardiovascular fibrosis to which older individuals are subjected, and thereby improve cardiovascular function and reduce the risk of cardiovascular associated mortality. Although the factors responsible for the anti-fibrotic action of CoQ10 have yet to be fully elucidated, its antioxidant and anti-inflammatory functions are thought to be major contributors to its clinical efficacy in the treatment of this age-related disorder.

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