The Combination of Selenium and Vitamin E Inhibits Type I Collagen Formation in Cultured Hepatic Stellate Cells

Mezey, Esteban; Liu, Xiaopu; Potter, James J.

doi:10.1007/s12011-010-8672-7

Cited by 9 publications

(7 citation statements)

References 33 publications

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“…In line with some studies, the result of the present work indicated that infection of mice with S. mansoni revealed obvious decrease in the non enzymatic antioxidant; GSH, as well as the enzymatic antioxidants including, GR, TrRx, and CAT (Gharib et al, 1999;EL-Sokkary et al, 2002). Treatment with the current micronutrients either alone or in combination, showed an improvement in the antioxidant biomarkers ensuring the antioxidant ability of these agents (Ben Amara et al, 2011;Mezey et al, 2011) The present work showed that the inflammatory reactions and tissue damage induced in livers of S. mansoni infected mice are ensured by marked increase in serum GGT and ALT levels and a decrease in albumin level ( Mohamed et al, 2008;Morais et al, 2010). The increment of such enzymes in serum may be due to the destruction of hepatocytes by the action of toxins of the parasite eggs leading to their release into the circulation (Cheever and Anderson, 1971).…”

Section: Discussionsupporting

confidence: 89%

Influence of some micronutrients and Citharexylum quadrangular extract against liver fibrosis in Schistosoma mansoni infected mice

Kadry¹

2013

Afr. J. Pharm. Pharmacol.

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Despite effective chemotherapy, schistosomiasis remains the second major public health problem in the developing world, second to malaria. The present study was undertaken to explore the therapeutic effect of the micronutrients (vitamin E and selenium) and chloroform extract of Citharexylum quadrangular leaves and their mixture against the deleterious pathological impacts induced in mice livers by Schistosoma mansoni infection. Parasitological markers showed that oral ingestion of the different supplements to S. mansoni infected mice was effective in reducing the worm burden with concomitant decrease in the egg burden, granuloma count and its diameter as well as total area of infection in their livers versus untreated ones. Parasitological parameters were reflected by the improvement of the histopathological pictures of livers of infected-treated mice. The current investigation also showed that the used agents and their mixture successfully modulated liver fibrosis of infected mice which was documented by a marked decrease of liver hydroxyproline level (as biomarker of liver fibrosis) as well as the serum levels of inflammatory fibrogenic mediators namely, fructosamine, tumor necrosis factor alpha (TNFα) and total immunoglobin E (IgE). In addition, the used agents showed ameliorative action on the elevated liver oxidative stress-nitric oxide (NO) and malondialdehyde (MDA) and the decreased antioxidant biomarkers, reduced glutathione (GSH), glutathione reductase (GR), thioredoxin reductase (TrxR) and catalase (CAT) which may have a role in liver damage and fibrosis due to S mansoni infection. In conclusion, treatment with the used micronutrients and plant extract either alone or in combination attenuated the deleterious impacts of S. mansoni infection on mice livers. The combination of all supplements was more effective as it greatly modified the inflammatory mediators and oxidative stress responsible for schistosomal liver fibrosis.

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Section: Discussionsupporting

confidence: 89%

Influence of some micronutrients and Citharexylum quadrangular extract against liver fibrosis in Schistosoma mansoni infected mice

Kadry¹

2013

Afr. J. Pharm. Pharmacol.

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“…Consistent with the role of SEPP1 in delivering Se to peripheral tissues for selenoprotein biosynthesis [89, 90], exogenous Se restored expression of GPX3 and TXNRD1 as well as TXNRD1 enzyme activity, depleted TGF β 1-induced ROS downstream of NOX4 induction, and inhibited myofibroblast differentiation of prostatic fibroblasts [26]. Similarly, exogenous Se also inhibited TGF β -mediated myofibroblast transdifferentiation of hepatic stellate cells [91]. Furthermore, we observed that exogenous Se restores morphological and molecular characteristics typical of the fibroblast phenotype to in vitro differentiated prostatic myofibroblasts even in the continued presence of the TGF β differentiation-inducing stimulus [4].…”

Section: Signaling By Nox4-derived Reactive Oxygen Species In the mentioning

confidence: 71%

Redox Signaling as a Therapeutic Target to Inhibit Myofibroblast Activation in Degenerative Fibrotic Disease

Sampson

Berger

Zenzmaier

2014

BioMed Research International

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Degenerative fibrotic diseases encompass numerous systemic and organ-specific disorders. Despite their associated significant morbidity and mortality, there is currently no effective antifibrotic treatment. Fibrosis is characterized by the development and persistence of myofibroblasts, whose unregulated deposition of extracellular matrix components disrupts signaling cascades and normal tissue architecture leading to organ failure and death. The profibrotic cytokine transforming growth factor beta (TGFβ) is considered the foremost inducer of fibrosis, driving myofibroblast differentiation in diverse tissues. This review summarizes recent in vitro and in vivo data demonstrating that TGFβ-induced myofibroblast differentiation is driven by a prooxidant shift in redox homeostasis. Elevated NADPH oxidase 4 (NOX4)-derived hydrogen peroxide (H2O2) supported by concomitant decreases in nitric oxide (NO) signaling and reactive oxygen species scavengers are central factors in the molecular pathogenesis of fibrosis in numerous tissues and organs. Moreover, complex interplay between NOX4-derived H2O2 and NO signaling regulates myofibroblast differentiation. Restoring redox homeostasis via antioxidants or NOX4 inactivation as well as by enhancing NO signaling via activation of soluble guanylyl cyclases or inhibition of phosphodiesterases can inhibit and reverse myofibroblast differentiation. Thus, dysregulated redox signaling represents a potential therapeutic target for the treatment of wide variety of different degenerative fibrotic disorders.

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“…In addition, it has been shown to inhibit the activity of ROS‐generating systems such as iNOS or NADPH oxidase . ROS have been identified as mediators in pulmonary or hepatic fibrosis and antioxidant supplementation has been used to reduce collagen deposition . For instance, Ibuki et al showed how oral supplementation with vitamin E in diabetic, obese mice reduced oxidative stress, decreased the expression of some MMPs and improved skin tensile strength and collagen fibers .…”

Section: Discussionmentioning

confidence: 99%

Vitamin E reduces adipose tissue fibrosis, inflammation, and oxidative stress and improves metabolic profile in obesity

Alcalá

Sánchez-Vera

Sevillano

et al. 2015

Obesity

106

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Objective: To test whether enhancing the capability of adipose tissue to store lipids using antioxidant supplementation may prevent the lipotoxic effects and improve the metabolic profile of long-term obesity. Methods: C57BL/6J mice were randomized into three experimental groups for 28 weeks: control group (n 5 10) fed chow diet (10% kcal from fat), obese group (O, n 5 12) fed high-fat (HF) diet (45% kcal from fat), and obese group fed HF diet and supplemented twice a week with 150 mg of a-tocopherol (vitamin E) by oral gavage (OE, n 5 12). Results: HF diet resulted in an obese phenotype with a marked insulin resistance, hypertriglyceridemia, and hepatic steatosis in O mice. Histological analysis of obese visceral adipose tissue (VAT) revealed smaller adipocytes surrounded by a fibrotic extracellular matrix and an increased macrophage infiltration, with the consequent release of proinflammatory cytokines. Vitamin E supplementation decreased oxidative stress and reduced collagen deposition in the VAT of OE mice, allowing a further expansion of the adipocytes and increasing the storage capability. As a result, circulating cytokines were reduced and hepatic steasosis, hypertriglyceridemia, and insulin sensitivity were improved. Conclusions: Our results suggest that oxidative stress is implicated in extracellular matrix remodeling and may play an important role in metabolic regulation.

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The Combination of Selenium and Vitamin E Inhibits Type I Collagen Formation in Cultured Hepatic Stellate Cells

Cited by 9 publications

References 33 publications

Influence of some micronutrients and Citharexylum quadrangular extract against liver fibrosis in Schistosoma mansoni infected mice

Influence of some micronutrients and Citharexylum quadrangular extract against liver fibrosis in Schistosoma mansoni infected mice

Redox Signaling as a Therapeutic Target to Inhibit Myofibroblast Activation in Degenerative Fibrotic Disease

Vitamin E reduces adipose tissue fibrosis, inflammation, and oxidative stress and improves metabolic profile in obesity

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