Blog Archives

Epidermal E-Cadherin Dependent β-Catenin Pathway Is Phytochemical Inducible and Accelerates Anagen Hair Cycling.

Ahmed NS, Ghatak S, El Masry MS, Gnyawali SC, Roy S, Amer M, Everts H, Sen CK, Khanna S

Mol Ther. 2017 Nov 1;25(11):2502-2512. doi: 10.1016/j.ymthe.2017.07.010. Epub 2017 Jul 20.

Abstract

Unlike the epidermis, which regenerates continually, hair follicles anchored in the subcutis periodically regenerate by spontaneous repetitive cycles of growth (anagen), degeneration (catagen), and rest (telogen). The loss of hair follicles in response to injuries or pathologies such as alopecia endangers certain inherent functions of the skin. Thus, it is of interest to understand mechanisms underlying follicular regeneration in adults. In this work, a phytochemical rich in the natural vitamin E tocotrienol (TRF) served as a productive tool to unveil a novel epidermal pathway of hair follicular regeneration. Topical TRF application markedly induced epidermal hair follicle development akin to that during fetal skin development. This was observed in the skin of healthy as well as diabetic mice, which are known to be resistant to anagen hair cycling. TRF suppressed epidermal E-cadherin followed by 4-fold induction of β-catenin and its nuclear translocation. Nuclear β-catenin interacted with Tcf3. Such sequestration of Tcf3 from its otherwise known function to repress pluripotent factors induced the plasticity factors Oct4, Sox9, Klf4, c-Myc, and Nanog. Pharmacological inhibition of β-catenin arrested anagen hair cycling by TRF. This work reports epidermal E-cadherin/β-catenin as a novel pathway capable of inducing developmental folliculogenesis in the adult skin.

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Palm vitamin E reduces locomotor dysfunction and morphological changes induced by spinal cord injury and protects against oxidative damage.

Zadeh-Ardabili PM, Rad SK, Rad SK, Khazaài H, Sanusi J, Zadeh MH

Sci Rep. 2017 Oct 30;7(1):14365. doi: 10.1038/s41598-017-14765-3.

Abstract

Spinal cord injury (SCI) occurs following different types of crushes. External and internal outcomes of SCI are including paralysis, cavity, and cyst formation. Effects of dietary derived antioxidants, such as palm vitamin E on central nervous system (CNS) encourage researchers to focus on the potential therapeutic benefits of antioxidant supplements. In the present study, experiments were carried out to evaluate the neuro-protective effect of the palm vitamin E on locomotor function and morphological damages induced SCI. Seventy-two male rats (Sprague-Dawley) were randomly divided into four groups: sham (laminectomy); control (supplemented with the palm vitamin E at a dose of 100 mg/kg/day); untreated-SCI (partial crush, 30-33% for 20 sec); treated-SCI (partial crush, 30-33% for 20 sec supplemented with the palm vitamin E at a dose of 100 mg/kg/day). The treatment with the palm vitamin E significantly improved the hind limb locomotor function, reduced the histopathological changes and the morphological damage in the spinal cord. Also, the palm vitamin E indicated a statistically significant decrease in the oxidative damage indicators, malondialdehyde (MDA) level and glutathione peroxidase (GPx) activity in the treated-SCI compared to the untreated-SCI.

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Vitamin E (α‑tocopherol) ameliorates aristolochic acid‑induced renal tubular epithelial cell death by attenuating oxidative stress and caspase‑3 activation.

Wu TK, Pan YR, Wang HF, Wei CW, Yu YL

Mol Med Rep. 2017 Oct 27. doi: 10.3892/mmr.2017.7921. [Epub ahead of print]

Abstract

Aristolochic acid (AA) is a component identified in traditional Chinese remedies for the treatment of arthritic pain, coughs and gastrointestinal symptoms. However, previous studies have indicated that AA can induce oxidative stress in renal cells leading to nephropathy. α‑tocopherol exists in numerous types of food, such as nuts, and belongs to the vitamin E isoform family. It possesses antioxidant activities and has been used previously for clinical applications. Therefore, the aim of the present study was to determine whether α‑tocopherol could reduce AA‑induced oxidative stress and renal cell cytotoxicity, determined by cell survival rate, reactive oxygen species detection and apoptotic features. The results indicated that AA markedly induced H2O2 levels and caspase‑3 activity in renal tubular epithelial cells. Notably, the presence of α‑tocopherol inhibited AA‑induced H2O2 and caspase‑3 activity. The present study demonstrated that antioxidant mechanisms of α‑tocopherol may be involved in the increased survival rates from AA‑induced cell injury.

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Vitamin E-Coated Dialyzer Inhibits Oxidative Stress.

Yamadera S, Nakamura Y, Inagaki M, Ohsawa I, Gotoh H, Goto Y, Sato N, Oguchi T, Gomi Y, Tsuji M, Kiuchi Y, Iwai S

Blood Purif. 2017 Oct 25;44(4):288-293. doi: 10.1159/000478971.

Abstract

AIM:

To examine the effects of vitamin E-coated dialyzer on oxidative stress in vitro.

METHODS:

A dialyzer with a synthetic polymer membrane (APS-11SA) and vitamin E-coated dialyzer (VPS-11SA) were connected to a blood tubing line, and U937 cells were circulated in the device. The circulating fluid was collected at 1, 2, 5, 10, 25, and 50 cycles, which are estimated numbers of passes through the dialyzer. Intracellular reactive oxygen species (ROS) production, malondialdehyde (MDA), and Cu/Zn-superoxide dismutase (SOD) were quantified.

RESULTS:

Intracellular ROS production was increased in the first cycle by APS-11SA and was decreased throughout the experiment by VPS-11SA. Intracellular ROS production in the VPS-11SA device was lower, and MDA levels were decreased. MDA levels were lower during VPS-11SA processing than during APS-11SA processing. Cu/Zn-SOD levels remained unchanged.

CONCLUSION:

Our results highlight anti-oxidative-stress effects of a vitamin E-coated dialyzer.

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Here’s why you should be taking vitamin E

Vitamin E sure tops the chart of our favourite beauty ingredients. It has intense hydrating and anti-ageing properties, and can work wonders on your skin and hair if applied regularly. We list down all the skin and hair concerns that Vitamin E can be used to fight against.

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Vitamin E Reversed Apoptosis of Cardiomyocytes Induced by Exposure to High Dose Formaldehyde During Mice Pregnancy.

Wu D, Jiang Z, Gong B, Dou Y, Song M, Song X, Tian Y

Int Heart J. 2017 Oct 21;58(5):769-777. doi: 10.1536/ihj.16-279.

Abstract

In this study, we investigated the protection effect of Vitamin E (Vit E) on formaldehyde (FA) exposure during pregnancy induced apoptosis of cardiomyocytes, and used an HL-1 cell line to confirmed the findings in vivo.Pregnant mice received different doses of FA (0.5 mg/kg, 1.0 mg/kg, 1.5 mg/kg, 0.1 μg Vit E, or 1.5 mg/kg + 0.1 μg Vit E). TUNEL staining was used to reveal the apoptosis in cardiomyocytes, and SOD, MDA, GSH, Livin, and Caspase-3 in cardiomyocytes were detected by ELISA, RT-PCR, and Western blot. For in vitro study, HL-1 cells were treated with vehicle, 5 μmol/L FA, 25 μmol/L FA, 50 μmol/L FA, 10 mg/L Vit. E, and 50 μmol/L FA+ 10 mg/L Vit E, respectively. CCK-8 assay and flow cytometry were used to evaluate cell vitality and apoptosis. A high dose of FA exposure led to cytotoxicity in both pregnant mice and offspring, as TUNEL staining revealed a significant apoptosis of cardiomyocytes, and the alternation in SOD, GSH, MDA, Livin, and Caspase-3 was found in cardiomyocytes. 0.1 μg Vit. E could reverse high doses of FA exposure induced apoptosis of cardiomyocytes in both pregnant mice and offspring. The in vitro study revealed that FA exposure induced a decrease of cell viability and increased cell apoptosis, as well as oxidative stress in HL-1 cells with alternation in SOD, GSH, MDA, Livin, and Caspase-3.This study revealed a high dose of FA induced oxidative stress and apoptosis of cardiomyocytes in both pregnant mice and offspring, and Vit E supplement during pregnancy reversed the systemic and myocardial toxicity of FA.

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Association of Vitamin E Levels with Metabolic Syndrome, and MRI-Derived Body Fat Volumes and Liver Fat Content.

Waniek S, di Giuseppe R, Plachta-Danielzik S, Ratjen I, Jacobs G, Koch M, Borggrefe J, Both M, Müller HP, Kassubek J, Nöthlings U, Esatbeyoglu T, Schlesinger S, Rimbach G, Lieb W

Nutrients. 2017 Oct 18;9(10). pii: E1143. doi: 10.3390/nu9101143.

Abstract

We aimed to relate circulating α- and γ-tocopherol levels to a broad spectrum of adiposityrelated traits in a cross-sectional Northern German study. Anthropometric measures were obtained, and adipose tissue volumes and liver fat were quantified by magnetic resonance imaging in 641 individuals (mean age 61 years; 40.6% women). Concentrations of α- and γ-tocopherol were measured using high performance liquid chromatography. Multivariable-adjusted linear and logistic regression were used to assess associations of circulating α- and γ-tocopherol/cholesterol ratio levels with visceral (VAT) and subcutaneous adipose tissue (SAT), liver signal intensity (LSI), fatty liver disease (FLD), metabolic syndrome (MetS), and its individual components. The α- tocopherol/cholesterol ratio was positively associated with VAT (β scaled by interquartile range (IQR): 0.036; 95%Confidence Interval (CI): 0.0003; 0.071) and MetS (Odds Ratio (OR): 1.83; 95% CI: 1.21-2.76 for 3rd vs. 1st tertile), and the γ-tocopherol/cholesterol ratio was positively associated with VAT (β scaled by IQR: 0.066; 95% CI: 0.027; 0.104), SAT (β scaled by IQR: 0.048; 95% CI: 0.010; 0.087) and MetS (OR: 1.87; 95% CI: 1.23-2.84 for 3rd vs. 1st tertile). α- and γ-tocopherol levels were positively associated with high triglycerides and low high density lipoprotein cholesterol levels (all Ptrend < 0.05). No association of α- and γ-tocopherol/cholesterol ratio with LSI/FLD was observed. Circulating vitamin E levels displayed strong associations with VAT and MetS. These observations lay the ground for further investigation in longitudinal studies.

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Vitamin E: A Closer Look at Tocotrienols

When vitamin E was discovered in 1922, it was discovered as alpha-tocopherol. Between that time and 1940, scientists delved into tocopherol research, ranging from alpha-tocopherol’s isolation from plants2, chemical identification3,4, complete synthesis5, and antioxidant activity6. In fact, the tocopherol form remained the main focus of vitamin E science for decades, and, as such, research on tocopherols boomed.7,8

Tocotrienols were discovered later, in the mid-1960s.9,10 Tocotrienols’ ability to lower lipids was first reported in the early 1980s; in the 1990s, tocotrienols were associated with reduction of cardiovascular diseases and inhibition of cancers.11 Despite the growing research on tocotrienols, they are still often confused with tocopherols and were not even properly listed in the Merck Index, the encyclopedia of chemicals, drugs, and biologicals, until 2001.12

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Does vitamin E prevent asthma or wheeze in children: A systematic review and meta-analysis.

Wu H, Zhang C, Wang Y, Li Y

Paediatr Respir Rev. 2017 Oct 16. pii: S1526-0542(17)30093-3. doi: 10.1016/j.prrv.2017.08.002.

Abstract

Asthma is a heterogeneous disease with multiple phenotypes. Epidemiologic studies suggest a close relationship between vitamin E and the occurrence of asthma, wheezing and atopic conditions during childhood. Previous results on its effects have been conflicting. The aim of this meta-analysis was to critically examine the current evidence on the association of vitamin E with childhood asthma and wheezing. We searched electronic databases for observational studies in English-language journals published from 2000 to 2016. The initial search found 420 titles; nineteen studies were eligible according to the abstracts and details, which included reporting asthma or wheeze as an outcome. None of the articles included in this meta-analysis reported side effects of vitamin E supplementation during pregnancy. This meta-analysis found that vitamin E supplementation during pregnancy influenced the risk of asthma. To better understand the effectiveness and safety of vitamin E in children with asthma, large-scale, well-designed and randomized controlled trials are needed.

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Antioxidative and haematoprotective activity of coenzyme Q10 and vitamin E against cadmium-induced oxidative stress in Wistar rats.

Paunović MG, Matić MM, Ognjanović BI, Saičić ZS

Toxicol Ind Health. 2017 Oct;33(10):746-756. doi: 10.1177/0748233717725480.

Abstract

Cadmium (Cd) is a major environmental pollutant, which exerts adverse effects mainly by inducing oxidative stress. Coenzyme Q10 (CoQ10) and vitamin E (VE), naturally occurring antioxidants, improve health condition by inactivating free radicals and enhancing antioxidative defence. The aim of our study was to investigate the protective role of CoQ10 and/or VE pretreatment against Cd-induced haematotoxicity. Wistar albino rats were intramuscularly injected with CoQ10 (20 mg/kg b.w.) and/or VE (20 IU/kg b.w.) or with saline (control group). After 24 h, Cd was injected intraperitoneally (0.4 mg/kg b.w.) and 1 day after, animals were sacrificed. Acute Cd intoxication caused significant changes in haematological and biochemical parameters and altered the glutathione cycle, leading to the formation of lipid peroxidation, while the concentrations and activities of antioxidants (vitamins C and E, superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase) were decreased. CoQ10 and/or VE significantly maintained these values to near-normal levels, afforded additional protection by reducing lipid peroxidation and improved the levels of antioxidants in the blood. Plasma CoQ10 and VE levels negatively correlated with oxidative damage parameters while positively correlated with antioxidative defence parameters. Regarding their effects, CoQ10 and VE were in synergistic interaction. The present study suggested that CoQ10 and VE combination may be beneficial in protecting from Cd-induced haematotoxicity and may be used as a preventive against acute Cd intoxication of exposed people.

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