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Astaxanthin as a Modulator of Nrf2, NF-κB, and Their Crosstalk: Molecular Mechanisms and Possible Clinical Applications

Journal

MOLECULES
Volume 27, Issue 2, Pages -

Publisher

MDPI
DOI: 10.3390/molecules27020502

Keywords

astaxanthin; oxidative stress; inflammation; Nrf2; NF-kappa B

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This article reviews the potential molecular mechanisms by which astaxanthin (AST) regulates the transcription factors Nrf2 and NF-κB, which are involved in oxidative stress and inflammation. Additionally, it summarizes the current clinical studies elucidating how AST alleviates the etiopathogenesis of oxidative stress and inflammation.
Astaxanthin (AST) is a dietary xanthophyll predominantly found in marine organisms and seafood. Due to its unique molecular features, AST has an excellent antioxidant activity with a wide range of applications in the nutraceutical and pharmaceutical industries. In the past decade, mounting evidence has suggested a protective role for AST against a wide range of diseases where oxidative stress and inflammation participate in a self-perpetuating cycle. Here, we review the underlying molecular mechanisms by which AST regulates two relevant redox-sensitive transcription factors, such as nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor kappa B (NF-kappa B). Nrf2 is a cellular sensor of electrophilic stress that coordinates the expression of a battery of defensive genes encoding antioxidant proteins and detoxifying enzymes. Likewise, NF-kappa B acts as a mediator of cellular stress and induces the expression of various pro-inflammatory genes, including those encoding cytokines, chemokines, and adhesion molecules. The effects of AST on the crosstalk between these transcription factors have also been discussed. Besides this, we summarize the current clinical studies elucidating how AST may alleviate the etiopathogenesis of oxidative stress and inflammation.

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