&lt;p&gt;Astaxanthin in Liver Health and Disease: A Potential Therapeutic Agent&lt;/p&gt;

Li, Jingjing; Guo, Chuanyong; Wu, Jianye

doi:10.2147/dddt.s230749

Cited by 55 publications

(42 citation statements)

References 89 publications

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“…In terms of burn injury, we observed that ATX exerted a protective effect against burn-induced early AKI by ameliorating oxidative damage and downregulating mitochondria-related apoptosis via the PI3K/Akt/Bad pathway 7 . Combined with similar reports of its effects on oxidative damage and inflammation in other organ injuries, ATX seems to be a promising and nontoxic therapeutic reagent to prevent early AKI after burn injury 20 , 21 .…”

Section: Introductionmentioning

confidence: 68%

“…Astaxanthin (ATX) is a natural and strong antioxidant that can be extracted from multiple crustaceans 32 . ATX is considered to be a safe and hopeful therapeutic agent in several diseases, as well as a safe feed additive and dietary supplement 21 , 33 – 35 . Our previous study primarily demonstrated the protective value of ATX in burn-induced early AKI, and the mechanism of action was found to be related to its ability to attenuate oxidative stress and secondary renal cell apoptosis 7 .…”

Section: Discussionmentioning

confidence: 99%

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Astaxanthin protects against early acute kidney injury in severely burned rats by inactivating the TLR4/MyD88/NF-κB axis and upregulating heme oxygenase-1

Guo

Fang

et al. 2021

Sci Rep

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Early acute kidney injury (AKI) contributes to severe morbidity and mortality in critically burned patients. Renal inflammation plays a vital role in the progression of early AKI, acting as a therapeutic target. Astaxanthin (ATX) is a strong antioxidant widely distributed in marine organisms that exerts many biological effects in trauma and disease. ATX is also suggested to have anti-inflammatory activity. Hence, we attempted to explore the role of ATX in protecting against early postburn AKI via its anti-inflammatory effects and the related mechanisms. A severely burned model was established for histological and biochemical assessments based on adult male rats. We found that oxidative stress-induced tissue inflammation participated in the development of early AKI after burn injury and that the MyD88-dependent TLR4/NF-κB pathway was activated to regulate renal inflammation. The TLR4 and NF-κB inhibitors TAK242 and PDTC showed similar effects in attenuating burn-induced renal inflammation and early AKI. Upon ATX treatment, the release of inflammatory mediators in the kidneys was downregulated, while the TLR4/MyD88/NF-κB axis was inhibited in a dose-related manner. TAK242 and PDTC could enhance the anti-inflammatory effect of high-dose ATX, whereas lipopolysaccharide (LPS) reversed its action. Furthermore, the expression of heme oxygenase (HO)-1 was upregulated by ATX in a dose-related manner. Collectively, the above data suggest that ATX protects against renal inflammation in a dose-related manner by regulating the TLR4/MyD88/NF-κB axis and HO-1 and ultimately prevents early AKI following severe burns.

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Section: Introductionmentioning

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Astaxanthin protects against early acute kidney injury in severely burned rats by inactivating the TLR4/MyD88/NF-κB axis and upregulating heme oxygenase-1

Guo

Fang

et al. 2021

Sci Rep

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“…Next, we need to explore the mechanisms of fenofibrate on how to attenuate the injury of IR. PPAR- α is a key transcription factor that mediates the nucleus–mitochondrial interactions to regulate inflammation, lipid metabolism, and mitochondrial functions in various tissues and cells, and it has become a main target in NFALD [ 36 , 37 ]. PPAR- α activation increases the expression of sirtuin-1 (SIRT1), which inhibits NF- κ B, depending on the AMPK pathway and thus reducing inflammation [ 38 , 39 ].…”

Section: Discussionmentioning

confidence: 99%

Fenofibrate Ameliorates Hepatic Ischemia/Reperfusion Injury in Mice: Involvements of Apoptosis, Autophagy, and PPAR-α Activation

et al. 2021

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Hepatic ischemia and reperfusion injury is characterized by hepatocyte apoptosis, impaired autophagy, and oxidative stress. Fenofibrate, a commonly used antilipidemic drug, has been verified to exert hepatic protective effects in other cells and animal models. The purpose of this study was to identify the function of fenofibrate on mouse hepatic IR injury and discuss the possible mechanisms. A segmental (70%) hepatic warm ischemia model was established in Balb/c mice. Serum and liver tissue samples were collected for detecting pathological changes at 2, 8, and 24 h after reperfusion, while fenofibrate (50 mg/kg, 100 mg/kg) was injected intraperitoneally 1 hour prior to surgery. Compared to the IR group, pretreatment of FF could reduce the inflammatory response and inhibit apoptosis and autophagy. Furthermore, fenofibrate can activate PPAR-α, which is associated with the phosphorylation of AMPK.

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“…Compared with β-carotene and vitamin E, AST has 10-fold and 100fold stronger antioxidant capacity, respectively (Li et al, 2020). In different experimental models, AST has a preventive effect on heart, kidney, lungs, and nerve injury through reducing oxidative stress in the organism (Ni et al, 2018;Xu et al, 2019;Yamagishi & Aihara, 2014).…”

Section: Introductionmentioning

confidence: 99%

Analysis of astaxanthin molecular targets based on network pharmacological strategies

Lin

Tan

et al. 2021

J Food Biochem

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In order to further explore the potential pharmacological activity of astaxanthin (AST), network pharmacological approaches were employed in this work to systematically investigate its affinity targets, perturbed signaling pathways, and related disease applications. First, potential targets were captured based on AST chemical structure information. Enrichment analysis was then performed using bioinformatics tools to predict the biological processes and diseases in which AST targets are involved. The results suggest that AST is involved in steroid hormone metabolism, and the regulation of glucocorticoids may be one of the potential mechanisms of its known therapeutic effects on depression and insulin resistance. Molecular docking experiments confirmed that AST can form stable binding to several key nodes (SRD5A2, STS, AKR1C2, HSD11B1, and CYP17A1) in steroid hormone biosynthesis.More importantly, the molecular targets of AST were the most significantly associated with endometriosis. Functionally, grouped analysis of key therapeutic nodes was carried out by establishing the interaction network between drug targets and disease targets. While exerting inflammatory effects, the regulation of estrogen and other semiochemicals by targeting steroid metabolism may be the biological basis for the potential treatment of endometriosis with AST. This work provides a theoretical basis for further exploring the pharmacological mechanisms of AST and development of new therapeutic applications. Practical applicationsIn this study, systematic pharmacological methods were used to identify the potential therapeutic effects and associated mechanisms of astaxanthin, providing a bioinformatics basis for further exploration of astaxanthin's new pharmacological properties in foods.

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<p>Astaxanthin in Liver Health and Disease: A Potential Therapeutic Agent</p>

Cited by 55 publications

References 89 publications

Astaxanthin protects against early acute kidney injury in severely burned rats by inactivating the TLR4/MyD88/NF-κB axis and upregulating heme oxygenase-1

Astaxanthin protects against early acute kidney injury in severely burned rats by inactivating the TLR4/MyD88/NF-κB axis and upregulating heme oxygenase-1

Fenofibrate Ameliorates Hepatic Ischemia/Reperfusion Injury in Mice: Involvements of Apoptosis, Autophagy, and PPAR-α Activation

Analysis of astaxanthin molecular targets based on network pharmacological strategies

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