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Entity

Name
alpha-tocopherol
Namespace
chebi
Namespace Version
20190224
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/c328ad964c08967a0417a887510b97b965a62fa5/external/chebi-names.belns

Appears in Networks 2

In-Edges 0

Out-Edges 14

a(CHEBI:"alpha-tocopherol") decreases p(HGNC:IL1B) View Subject | View Object

Furthermore, it disrupted the activity of NF-B, and thus, caused the suppression of NO synthase and inflammatory regulators such as IL-6 and IL-1, and the reduction of microglial activation [37] PubMed:29179999

a(CHEBI:"alpha-tocopherol") decreases bp(GO:"microglial cell activation") View Subject | View Object

Furthermore, it disrupted the activity of NF-B, and thus, caused the suppression of NO synthase and inflammatory regulators such as IL-6 and IL-1, and the reduction of microglial activation [37] PubMed:29179999

a(CHEBI:"alpha-tocopherol") decreases a(CHEBI:"reactive oxygen species") View Subject | View Object

It has antiox-idant effects via the interference of reactive components and ROS by redox cycling of quinine, and subsequently generating hydroquinone [209]. PubMed:29179999

a(CHEBI:"alpha-tocopherol") decreases a(CHEBI:"amyloid-beta") View Subject | View Object

Reduction of A expression and cytotoxic-ity stimulated by A in neuroblastoma cells and the inhibition of inflammatory cytokines, ROS and NO in microglial cells were detected upon treatment with -tocopherol [210]. PubMed:29179999

a(CHEBI:"alpha-tocopherol") decreases a(CHEBI:"amyloid-beta") View Subject | View Object

Oxidative stress and A expression were suppressed with -tocopherol in mouse model. PubMed:29179999

a(CHEBI:"alpha-tocopherol") decreases a(MESH:Cytokines) View Subject | View Object

Reduction of A expression and cytotoxic-ity stimulated by A in neuroblastoma cells and the inhibition of inflammatory cytokines, ROS and NO in microglial cells were detected upon treatment with -tocopherol [210]. PubMed:29179999

a(CHEBI:"alpha-tocopherol") decreases a(CHEBI:"nitric oxide") View Subject | View Object

Reduction of A expression and cytotoxic-ity stimulated by A in neuroblastoma cells and the inhibition of inflammatory cytokines, ROS and NO in microglial cells were detected upon treatment with -tocopherol [210]. PubMed:29179999

a(CHEBI:"alpha-tocopherol") increases bp(GO:memory) View Subject | View Object

Memory defi-ciencies were improved by -tocopherol in transgenic mice. PubMed:29179999

a(CHEBI:"alpha-tocopherol") decreases path(MESH:"Oxidative Stress") View Subject | View Object

Oxidative stress and A expression were suppressed with -tocopherol in mouse model. PubMed:29179999

a(CHEBI:"alpha-tocopherol") decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Furthermore, it disrupted the activity of NF-B, and thus, caused the suppression of NO synthase and inflammatory regulators such as IL-6 and IL-1, and the reduction of microglial activation [37] PubMed:29179999

a(CHEBI:"alpha-tocopherol") decreases p(HGNC:NOS2) View Subject | View Object

Furthermore, it disrupted the activity of NF-B, and thus, caused the suppression of NO synthase and inflammatory regulators such as IL-6 and IL-1, and the reduction of microglial activation [37] PubMed:29179999

a(CHEBI:"alpha-tocopherol") decreases p(HGNC:IL6) View Subject | View Object

Furthermore, it disrupted the activity of NF-B, and thus, caused the suppression of NO synthase and inflammatory regulators such as IL-6 and IL-1, and the reduction of microglial activation [37] PubMed:29179999

a(CHEBI:"alpha-tocopherol") decreases a(MESH:"Reactive Oxygen Species") View Subject | View Object

As expected, α-tocopherol treatment prevented ROS accumulation and the induction of anti-oxidant genes in the heart (Figure 6A, B and see Figure 8 in [37]). PubMed:28400318

Appears in Networks:
Annotations
Cell Ontology (CL)
regular cardiac myocyte
Text Location
Results

a(CHEBI:"alpha-tocopherol") decreases bp(MESH:"Lipid Peroxidation") View Subject | View Object

Consistently, we measured increased lipid peroxidation in both cells and tissues exposed to free heme, which can be rescued by α-tocopherol, an agent able to react with lipid radicals and interrupt the oxidation reaction. PubMed:28400318

Appears in Networks:
Annotations
Cell Ontology (CL)
regular cardiac myocyte
Text Location
Discussion

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.