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Journal ArticleDOI

Diallyl sulfide induces heme oxygenase-1 through MAPK pathway

TLDR
It is found that DAS can induce the expression of heme oxygenase-1 (HO-1), which plays a critical role in the cell defense system against oxidative stress and protected the HepG2 cells against toxicity by hydrogen peroxide or arachidonic acid.
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This article is published in Archives of Biochemistry and Biophysics.The article was published on 2004-12-15. It has received 130 citations till now. The article focuses on the topics: MAPK/ERK pathway & Heme oxygenase.

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Glutathione Homeostasis and Functions: Potential Targets forMedical Interventions

TL;DR: The principal mechanisms of the protective role of GSH against reactive species and electrophiles are characterized and a hypothesis for investigation of the physiology and biochemistry of glutathione is provided with a focus on human and animal health.
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Nrf2 as a master redox switch in turning on the cellular signaling involved in the induction of cytoprotective genes by some chemopreventive phytochemicals.

TL;DR: This review highlights the cytoprotective gene expression induced by some representative dietary chemopreventive phytochemicals with the Nrf2-Keap1 system as a prime molecular target.
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Dual roles of Nrf2 in cancer

TL;DR: In response to oxidative stress, the transcription factor NF-E2-related factor 2 (Nrf2) controls the fate of cells through transcriptional upregulation of antioxidant response element (ARE)-bearing genes, including those encoding endogenous antioxidants, phase II detoxifying enzymes, and transporters.
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Role of oxidative stress in alcohol-induced liver injury

TL;DR: This review summarizes some of the leading pathways and discusses the evidence for their contribution to alcohol-induced liver injury, special emphasis is placed on CYP2E1, which is induced by alcohol and is reactive in metabolizing and activating many hepatotoxins, including ethanol, to reactive products, and in generating ROS.
Journal ArticleDOI

Hydrogen sulfide inhibits nitric oxide production and nuclear factor-κB via heme oxygenase-1 expression in RAW264.7 macrophages stimulated with lipopolysaccharide

TL;DR: The results suggest that H(2)S can inhibit NO production and NF-kappaB activation in LPS-stimulated macrophages through a mechanism that involves the action of HO-1/CO.
References
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Journal ArticleDOI

THE HEME OXYGENASE SYSTEM:A Regulator of Second Messenger Gases

TL;DR: This review highlights the current information on molecular and biochemical properties of HO-1 and HO-2 and addresses the possible mechanisms for mutual regulatory interactions between the CO- and NO-generating systems.
Journal ArticleDOI

Nrf2, a Cap'n'Collar transcription factor, regulates induction of the heme oxygenase-1 gene.

TL;DR: Results implicate Nrf2 in the induction of the HO-1 gene but suggest that the NRF2 partner in this function is a factor other than p18 or Jun proteins.
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Heme oxygenase-1: function, regulation, and implication of a novel stress-inducible protein in oxidant-induced lung injury.

TL;DR: The magnitude ofHO-1 induction after oxidative stress and the wide distribution of this enzyme in systemic tissues coupled with the intriguing biological activities of the catalytic byproducts, carbon monoxide, iron, and bilirubin makes HO-1 a highly attractive and interesting candidate stress-response protein which may play key role(s) in mediating protection against oxidant-mediated lung injury.
Journal ArticleDOI

Heme oxygenase/carbon monoxide signaling pathways: regulation and functional significance.

TL;DR: Recent progress indicates that CO exerts novel anti-inflammatory and anti-apoptotic effects dependent on the modulation of the p38 mitogen activated protein kinase (MAPK)-signaling pathway, and likely plays a role in HO-1 mediated tissue protection.
Journal ArticleDOI

Transcriptional regulation of the heme oxygenase-1 gene via the stress response element pathway.

J Alam, +1 more
TL;DR: Detailed analysis of the mouse gene, and to a lesser extent of the human gene, has identified a common mechanism the stress response element (StRE)/Nrf2 transcription factor pathway for gene regulation in response to a diverse array of HO-1 inducers including the substrate heme, various environmental and industrial toxins, and plant-derived polyphenolic compounds.
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