Study on the relationship between astaxanthin and human health

Astaxanthin is a terpene unsaturated compound, widely present in the biological world. It is also a chain-breaking antioxidant with strong antioxidant capacity. It can remove nitrogen dioxide, sulfide, disulfide, etc. It can also reduce lipid peroxidation and effectively inhibit lipid peroxidation caused by free radicals. At the same time, astaxanthin has many physiological effects such as inhibiting tumor occurrence, enhancing immunity, and removing free radicals in the body. It has a good therapeutic effect on skin cancer caused by ultraviolet rays and prevents and treats eye diseases caused by diabetes. It has broad application prospects in health products, medicine, cosmetics, food additives and aquaculture. Exploring the benefits of astaxanthin to human health is conducive to the comprehensive utilization of astaxanthin resources and enhancing economic value.

Research results sharing

01 Astaxanthin targets IL-6 and reduces LPS-induced adverse inflammatory responses of macrophages

Abstract

Astaxanthin (AST) is an effective carotenoid antioxidant, and its anti-inflammatory mechanism and specific molecular targets are relatively less studied. In this study, human monocytic leukemia cell-derived macrophages (THP-1) were selected as experimental cells, and lipopolysaccharide (LPS) was used as an inflammatory stimulus. After LPS treatment, oxidative stress increased significantly, accompanied by significant cell damage. In addition, LPS also increased the expression of inflammation-related molecules. The experimental results showed that AST intervention can effectively alleviate LPS-induced oxidative stress, promote cell repair, and significantly reduce inflammation. Further exploration of the anti-inflammatory mechanism found that AST can significantly inhibit the translocation and activation of NF-κB, and reduce the production of inflammatory factors by hindering NF-κB through antioxidant mechanisms. The experiment further confirmed that AST has a protective effect on cell damage and reduces the damage of inflammatory cytokines by activating p53 and inhibiting STAT3. In addition, using network pharmacology and computer calculations based on molecular docking and molecular dynamics simulation, interleukin 6 (IL-6) was determined to be an important core target of AST anti-inflammatory, and further verified by RNA interference experiments. This IL-6 binding ability actually enables AST to inhibit the positive cycle of inflammatory factors and avoid possible inflammation. Therefore, this study provides new possibilities for the application and development of astaxanthin as a popular dietary supplement with anti-inflammatory or immunomodulatory functions.

Conclusion

Astaxanthin targets IL-6 and inhibits LPS-induced adverse inflammatory responses in macrophages. In summary, the results of the experiment showed that AST exhibited anti-oxidative stress, anti-cell damage, and anti-inflammatory effects on LPS-stimulated macrophages. AST protected cells from damage, stimulated p53, inhibited STAT3, and alleviated inflammatory factors caused by damage. The study also confirmed that AST inhibited NF-κB and reduced the production of inflammatory factors through antioxidant mechanisms. IL-6 is the key core target of AST's anti-inflammatory effect. Therefore, it is proposed that AST can effectively inhibit the positive feedback of inflammatory factors and prevent the occurrence of inflammatory spread.

02 Astaxanthin improves CTX-induced skeletal muscle regeneration in HFD-fed obese mice through mitochondrial biosynthesis

Abstract

Obesity impairs the health and regeneration of skeletal muscle. Astaxanthin (AX) has antioxidant and anti-obesity properties and can improve obesity-related damage. Forty-two male C57BL/6J mice were fed a control diet, a high-fat diet (HFD), or a HFD containing 0.02% AX for 16 weeks. The mice were euthanized immediately (experiment 1), injected intramuscularly with cardiotoxin (CTX), and euthanized on the seventh day (experiment 2). Experiment 1 showed that AX could improve grip strength and motor function in rats, while reducing fat deposition and increasing SOD in skeletal muscle. Experiment 2 found that AX increased the expression of proteins related to muscle regeneration and mitochondrial biogenesis. In vitro experiments using AX to interfere with C2C12 myogenic cells showed that AX promoted myoblast differentiation and mitochondrial biogenesis. In conclusion, astaxanthin can improve skeletal muscle health and regeneration in HFD-induced obese mice.

Conclusion

This study showed that AX treatment can reduce subcutaneous fat accumulation in HFD-induced obese mice, improve lipid metabolism disorders in obese mice, reduce systemic inflammation and oxidative stress levels, enhance skeletal muscle function, and reduce ectopic lipid deposition in skeletal muscle. In addition, AX promotes mitochondrial biogenesis to improve skeletal muscle regeneration in obese mice. In summary, based on the current findings of the experiment, it is suggested that AX has the potential to alleviate skeletal muscle dysfunction in HFD-induced obesity, including enhancing skeletal muscle function and reducing ectopic lipid deposition in skeletal muscle. In addition, AX can improve skeletal muscle regeneration after CTX-induced muscle injury in HFD-fed obese mice. In vitro studies have shown that AX promotes myofibroblast differentiation, and this beneficial effect of promoting normal regeneration may be attributed to the enhancement of mitochondrial biogenesis.

03Astaxanthin inhibits renal clear cell carcinoma metastasis by scavenging reactive oxygen species

Abstract

Clear cell renal cell carcinoma (ccRCC) is a common form of renal cancer, and its poor prognosis is closely related to the occurrence of metastasis. ROS can drive epithelial-mesenchymal transition (EMT), thereby promoting cancer metastasis. Astaxanthin (AXT) is known for its excellent antioxidant properties, and this study shows that it can inhibit ccRCC metastasis by scavenging ROS. AXT dose-dependently reduced ROS levels and attenuated the migration and invasion ability of ccRCC cells. Furthermore, ccRCC cells treated with AXT exhibited phenotypic features indicative of EMT inhibition, as reflected by increased E-cadherin and decreased vimentin. Moreover, AXT-induced inhibition of metastatic potential was also confirmed in a mouse lung metastasis model. Notably, artificially increasing ROS levels reversed the AXT-induced reduction in migration and invasion capacity. Altogether, these findings highlight the anti-metastatic function of AXT in ccRCC, suggesting its therapeutic potential in treating ccRCC metastasis.

Conclusion

In this study, it was demonstrated that the anti-metastatic effect of AXT was established on ROS elimination, followed by blocking epithelial-mesenchymal transition (EMT) and attenuating the metastatic potential of ccRCC cells. The anti-metastatic function of AXT was demonstrated based on AXT-mediated inhibition of cell migration and invasion, EMT, and metastatic capacity in vivo. Furthermore, this experiment also demonstrated that AXT exerts its anti-metastatic effect through its ROS scavenging potential. ROS can regulate functional molecules (e.g., microRNAs, transcription factors) or signaling pathways associated with cancer progression, and AXT is known for its ROS scavenging. Therefore, it is reasonable to infer that the anticancer activity of AXT originates largely from its effects on ROS in cancer cells, making it a multifaceted carotene-like substance involved in a variety of biological processes.

Email: anna@hihealthbio.com

Cell/Wechat/Whatsapp: +86 17809202908

Tel: 0086-29-81142779