Astaxanthin as a Potential Neuroprotective Agent for Neurological Diseases

Haijian Wu, Huanjiang Niu, Anwen Shao, Cheng Wu, Brandon J Dixon, Jianmin Zhang, Shuxu Yang, Yirong Wang, Haijian Wu, Huanjiang Niu, Anwen Shao, Cheng Wu, Brandon J Dixon, Jianmin Zhang, Shuxu Yang, Yirong Wang

Abstract

Neurological diseases, which consist of acute injuries and chronic neurodegeneration, are the leading causes of human death and disability. However, the pathophysiology of these diseases have not been fully elucidated, and effective treatments are still lacking. Astaxanthin, a member of the xanthophyll group, is a red-orange carotenoid with unique cell membrane actions and diverse biological activities. More importantly, there is evidence demonstrating that astaxanthin confers neuroprotective effects in experimental models of acute injuries, chronic neurodegenerative disorders, and neurological diseases. The beneficial effects of astaxanthin are linked to its oxidative, anti-inflammatory, and anti-apoptotic characteristics. In this review, we will focus on the neuroprotective properties of astaxanthin and explore the underlying mechanisms in the setting of neurological diseases.

Keywords: apoptosis; astaxanthin; inflammation; neurological diseases; neuroprotection; oxidative stress.

Figures

Figure 1
Figure 1
The anti-oxidative effects of astaxanthin in neurological diseases. Astaxanthin facilitates the dissociation and nuclear translocation of nuclear erythroid 2-related factor (Nrf2), through activation of the PI3K/Akt and ERK signaling pathways, which contributes to increased expression of Nrf2-regulated enzymes like HO-1, NQO-1, and GST-α1 that resist oxidative stress. In addition, astaxanthin negatively regulates Sp1/NR1 signaling pathway, alleviating the production of intracellular ROS and oxidative stress.
Figure 2
Figure 2
The anti-inflammatory effects of astaxanthin in neurological diseases. Through suppression of IκB-α degradation and NF-κB nuclear translocation, astaxanthin inhibits the expression of inflammatory molecules IL-6, ICAM-1, and MCP1. Astaxanthin also suppresses nuclear expression of NF-κB and reduces downstream production of pro-inflammatory cytokines by restoring physiological levels of SHP-1.
Figure 3
Figure 3
The anti-apoptotic effects of astaxanthin in neurological diseases. Astaxanthin induces the activation of PI3K/Akt survival pathway, promoting the phosphorylation-dependent inactivation of Bad, which leads to a decrease in caspase-dependent neuronal apoptosis. Astaxanthin also maintains mitochondria integrity through modulation of p38 and MEK signaling pathways, which reduces cytochrome c release and inhibits caspase-dependent apoptotic cell death.

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Source: PubMed

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