Sulforaphane inhibition of monocyte adhesion via the suppression of ICAM-1 and NF-kappaB is dependent upon glutathione depletion in endothelial cells. (Q46772747)

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English	Sulforaphane inhibition of monocyte adhesion via the suppression of ICAM-1 and NF-kappaB is dependent upon glutathione depletion in endothelial cells.	scientific article

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2 January 2020

Sulforaphane inhibition of monocyte adhesion via the suppression of ICAM-1 and NF-kappaB is dependent upon glutathione depletion in endothelial cells (English)

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Yen-Chin Liu

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2 January 2020

Chia-Wen Hsieh

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Yu-Chun Weng

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Cheng-Yuan Hsieh

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Being-Sun Wung

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1 January 2008

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Vascular Pharmacology

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2 January 2020

A non-isotopic, highly sensitive, fluorimetric, cell-cell adhesion microplate assay using calcein AM-labeled lymphocytes

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Nuclear factor kappa B is a molecular target for sulforaphane-mediated anti-inflammatory mechanisms.

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Monochlorobimane fluorometric method to measure tissue glutathione

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Inflammation in atherosclerosis

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Chalcone inhibits the activation of NF-kappaB and STAT3 in endothelial cells via endogenous electrophile

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Constitutive and beta-naphthoflavone-induced expression of the human gamma-glutamylcysteine synthetase heavy subunit gene is regulated by a distal antioxidant response element/TRE sequence

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Molecular basis for the direct inhibition of AP-1 DNA binding by 15-deoxy-Delta 12,14-prostaglandin J2.

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Resveratrol suppresses IL-6-induced ICAM-1 gene expression in endothelial cells: effects on the inhibition of STAT3 phosphorylation

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15-Deoxy-Delta(12,14)-prostaglandin J(2) suppresses IL-6-induced STAT3 phosphorylation via electrophilic reactivity in endothelial cells

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10.1016/J.VPH.2007.11.006

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2 January 2020

PubMed publication ID

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Europe PubMed Central

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2 January 2020

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