Dosis: 3-18 mg/Tag
12. Bakterielle Infektionen
15. Degenerative Augenkrankheiten
17. Kognitive Schwäche
Supplementating with dietary astaxanthin combined with collagen hydrolysate improves facial elasticity and decreases matrix metalloproteinase-1 and -12 expression: a comparative study with placebo
The supplement group showed significant improvements in skin elasticity and transepidermal water loss in photoaged facial skin after 12 weeks compared with the placebo group. In the supplement group, expression of procollagen type I mRNA increased and expression of MMP-1 and -12 mRNA decreased compared with those in the placebo group. In contrast, there was no significant difference in UV-induced DNA damage between groups. These results demonstrate that dietary astaxanthin combined with collagen hydrolysate can improve elasticity and barrier integrity in photoaged human facial skin, and such treatment is well tolerated.
Protective effects of astaxanthin on skin deterioration
Participants were orally administered either a 6 mg or 12 mg dose of astaxanthin or a placebo. Wrinkle parameters and skin moisture content significantly worsened in the placebo group after 16 weeks. However, significant changes did not occur in the astaxanthin groups. Interleukin-1α levels in the stratum corneum significantly increased in the placebo and low-dose groups but not in the high-dose group between weeks 0 and 16. This study was performed in Japan from August to December, when changing environmental factors, such as UV and dryness, exacerbate skin deterioration. In conclusion, our study suggests that long-term prophylactic astaxanthin supplementation may inhibit age-related skin deterioration and maintain skin conditions associated with environmentally induced damage via its anti-inflammatory effect.
The Effects of a Dietary Supplement Containing Astaxanthin on Skin Condition
We studied the effect on the human skin of astaxanthin, which possess a strong anti-oxidative property, by oral administration in a single blind placebo controlled clinical test. Consequently, significant improvements by astaxanthin supplementation were observed in fine lines/wrinkles and elasticity by dermatologist’s visual assessment and in the moisture content by instrumental assessment at week 6. It seems that astaxanthin may protect the fresh collagen from oxidative stress such as singlet oxygen induced by UV. Placebo-effect or canola oil may improve moisture content in the placebo group.
Systematic Review and Meta-Analysis on the Effects of Astaxanthin on Human Skin Ageing
Oral ASX supplementation significantly restored moisture content (SMD = 0.53; 95% CI = 0.05, 1.01; I2 = 52%; p = 0.03) and improved elasticity (SMD = 0.77; 95% CI = 0.19, 1.35; I2 = 75%; p = 0.009) but did not significantly decrease wrinkle depth (SMD = −0.26; 95% CI = −0.58, 0.06; I2 = 0%; p = 0.11) compared to placebo. Open-label, prospective studies suggested slightly protective effects of topical and oral-topical ASX applications on skin ageing. Conclusions: Ingestion and/or topical usages of ASX may be effective in reducing skin ageing and have promising cosmetical potential, as it improves moisture content and elasticity and reduces wrinkles.
The effectiveness of a standardized rose hip powder, containing seeds and shells of Rosa canina, on cell longevity, skin wrinkles, moisture, and elasticity
In the double-blinded study, the rose hip group showed statistically significant improvements in crow’s-feet wrinkles (P<0.05), skin moisture (P<0.05), and elasticity (P<0.05) after 8 weeks of treatment. A similar improvement was observed for astaxanthin, with P-values 0.05, 0.001, and 0.05. Likewise, both groups expressed equal satisfaction with the results obtained in their self-assessment. The rose hip powder further resulted in increased cell longevity of erythrocyte cells during storage for 5 weeks in a blood bank.
Astaxanthin as a Putative Geroprotector: Molecular Basis and Focus on Brain Aging
Astaxanthin has been observed to slow down brain aging by increasing brain-derived neurotrophic factor (BDNF) levels in the brain, attenuating oxidative damage to lipids, protein, and DNA and protecting mitochondrial functions. Emerging data now suggest that ASX can modulate Nrf2, FOXO3, Sirt1, and Klotho proteins that are linked to longevity. Together, these mechanisms provide support for a role of ASX as a potential geroneuroprotector.
Astaxanthin alleviates pathological brain aging through the upregulation of hippocampal synaptic proteins
These findings suggest that astaxanthin can regulate the expression of synaptic proteins in mouse hippocampus through the sirtuin 1/peroxisome proliferator-activated receptor-γ coactivator 1α signaling pathway, which leads to improvements in the learning, cognitive, and memory abilities of mice.
Assessing the Potential of Nutraceuticals as Geroprotectors on Muscle Performance and Cognition in Aging Mice
On the other hand, both AX and krill oil supplementation increased force production without altering calcium homeostasis during excitation-contraction coupling mechanism or mitochondrial calcium uptake processes. We also provide evidence of improved spatial memory and learning ability in aging mice because of krill oil supplementation. Taken together, our data favors the application of antioxidant nutraceuticals as geroprotectors to improve cognition and healthy aging by virtue of improved skeletal muscle force production.
Building strength, endurance, and mobility using an astaxanthin formulation with functional training in elderly
Here, we show that functionally based exercise training combined with a formulation of natural anti‐inflammatory and antioxidant compounds improved muscle strength and size in elderly subjects more than exercise training alone. This was done without sacrificing the improvements in walking distance and endurance that typically accompany endurance training. These results suggest that the potential for strength and endurance improvements in elderly muscle is realized when natural products that promote adaptation are combined with exercise training incorporating both resistance and aerobic components. The end result is an approach involving functional exercise and a dietary formulation that can improve endurance, strength, and function to remedy the deficits associated with sarcopenia that limit mobility in the elderly.
Astaxanthin supplementation enhances metabolic adaptation with aerobic training in the elderly
In summary, AX is natural antioxidant and anti‐inflammatory supplement that may have the potential to benefit muscle function and exercise tolerance in the aged population. Here we have demonstrated that combining AX and exercise training leads to improved fat oxidation, CHO sparing, and increased exercise efficiency in aged healthy subjects, especially in males. These metabolic improvements combined with the benefits of the combined intervention on improvements in muscle strength, size, and specific force indicate that incorporation of AX into an exercise training program in the elderly could enhance exercise tolerance and quality of life. While these results are intriguing, the mechanisms underlying the enhanced adaptation to exercise and sex‐specific effects on fuel selection and exercise efficiency observed in this study are still unknown. Studies combining exercise training, functional testing, and adaptive signaling will be necessary to better understand the mechanisms by which AX enhances the adaptive response to training in aged subjects.
Potential of natural astaxanthin in alleviating the risk of cytokine storm in COVID-19
Here, we summarize the mounting evidence where ASX is shown to exert protective effect by regulating the expression of pro-inflammatory factors IL-1β, IL-6, IL-8 and TNF-α. We present reports where ASX is shown to prevent against oxidative damage and attenuate exacerbation of the inflammatory responses by regulating signaling pathways like NF-ĸB, NLRP3 and JAK/STAT. These evidences provide a rationale for considering natural astaxanthin as a therapeutic agent against inflammatory cytokine storm and associated risks in COVID-19 infection and this suggestion requires further validation with clinical studies.
Effect of Astaxanthin Supplementation on Salivary IgA, Oxidative Stress, and Inflammation in Young Soccer Players
This study indicates that Asx supplementation improves sIgA response and attenuates muscle damage, thus preventing inflammation induced by rigorous physical training. Our findings also point that Asx could show significant physiologic modulation in individuals with mucosal immunity impairment or under conditions of increased oxidative stress and inflammation.
Antioxidant and anti-inflammatory mechanisms of action of astaxanthin in cardiovascular diseases (Review)
Considering the potential beneficial effects of astaxanthin on cardiovascular health evidenced by preclinical and clinical studies, the aim of the present review was to describe the molecular and cellular mechanisms associated with the antioxidant and anti-inflammatory properties of this carotenoid in cardiovascular diseases, particularly atherosclerosis. The beneficial properties and safety profile of astaxanthin indicate that this compound may be used for preventing progression or as an adjuvant in the treatment of cardiovascular diseases.
Astaxanthin attenuates hepatic damage and mitochondrial dysfunction in non‐alcoholic fatty liver disease by up‐regulating the FGF21/PGC‐1α pathway
The results indicated that astaxanthin attenuated HFD‐ and FFA‐induced lipid accumulation and its associated oxidative stress, cell apoptosis, inflammation, and fibrosis both in vivo and in vitro. Astaxanthin up‐regulated FGF21 and PGC‐1α expression in damaged hepatocytes, which suggested an unrecognized mechanism of astaxanthin on ameliorating NAFLD. Astaxanthin attenuated hepatocyte damage and mitochondrial dysfunction in NAFLD by up‐regulating FGF21/PGC‐1α pathway. Our results suggest that astaxanthin may become a promising drug to treat or relieve NAFLD.
Astaxanthin Suppresses Cigarette Smoke-Induced Emphysema through Nrf2 Activation in Mice
Significantly increased expression levels of Nrf2 and its target gene, heme oxygenase-1 (HO-1), were found in the lung homogenates of astaxanthin-fed mice. The number of inflammatory cells in the bronchoalveolar lavage fluid (BALF) was significantly decreased, and emphysema was significantly suppressed. In conclusion, astaxanthin protects against oxidative stress via Nrf2 and ameliorates cigarette smoke-induced emphysema. Therapy with astaxanthin directed toward activating the Nrf2 pathway has the potential to be a novel preventive and therapeutic strategy for COPD.
Astaxanthin-Shifted Gut Microbiota Is Associated with Inflammation and Metabolic Homeostasis in Mice
BCO2 KO but not WT mice fed astaxanthin had ∼10-fold more of this compound in liver than controls (P < 0.05). In terms of the microbiota composition, deletion of BCO2 was associated with a significantly increased abundance of Mucispirillum schaedleri in mice regardless of gender. In addition to more liver astaxanthin in male KO compared with WT mice fed astaxanthin, the abundance of gut Akkermansia muciniphila was 385% greater, plasma glucagon-like peptide 1 was 27% greater, plasma glucagon and IL-1β were 53% and 30% lower, respectively, and colon NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome activation was 23% lower (all P < 0.05) in male KO mice than the WT mice.
Potential Anti-Atherosclerotic Properties of Astaxanthin
Astaxanthin has been reported to inhibit low-density lipoprotein (LDL) oxidation and to increase high-density lipoprotein (HDL)-cholesterol and adiponectin levels in clinical studies. Accumulating evidence suggests that astaxanthin could exert preventive actions against atherosclerotic cardiovascular disease (CVD) via its potential to improve oxidative stress, inflammation, lipid metabolism, and glucose metabolism. In addition to identifying mechanisms of astaxanthin bioactivity by basic research, much more epidemiological and clinical evidence linking reduced CVD risk with dietary astaxanthin intake is needed.
Astaxanthin Counteracts Vascular Calcification In Vitro Through an Early Up-Regulation of SOD2 Based on a Transcriptomic Approach
In conclusion, we demonstrated for the first time that astaxanthin could be a potential candidate treatment for VC, through inducing the up-regulation of SOD2 early during calcification progression and potentially suppressing vascular senescence.
Astaxanthin as a Potential Neuroprotective Agent for Neurological Diseases
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.
Anti-Tumor Effects of Astaxanthin by Inhibition of the Expression of STAT3 in Prostate Cancer
Astaxanthin resulted in suppression of the proliferation of DU145 cells and the level of STAT3. The treatment of DU145 cells with astaxanthin decreased the cloning ability, increased the apoptosis percentage and weakened the abilities of migration and invasion of the cells. Furthermore, astaxanthin reduced the expression of STAT3 at protein and mRNA levels. The effects were enhanced when astaxanthin and si-STAT3 were combined. The results of animal experiments were consistent with the results in cells. Thus, astaxanthin inhibits the proliferation of DU145 cells by reducing the expression of STAT3.
Astaxanthin Inhibits PC-3 Xenograft Prostate Tumor Growth in Nude Mice
The intervention was started when tumors reached 0.5–0.6 cm in diameter. Mice were intragastrically administered 100 mg/kg astaxanthin (HA), 25 mg/kg astaxanthin (LA), or olive oil (TC). The results showed that 100 mg/kg astaxanthin significantly inhibited tumor growth compared to the TC group, with an inhibitory rate of 41.7%. A decrease of Ki67 and proliferating cell nuclear antigen (PCNA) as well as an increase of cleaved caspase-3 were observed in HA-treated tumors, along with increasing apoptotic cells, obtained by TUNEL assay. The HA significantly elevated the levels of tumor suppressors miR-375 and miR-487b in tumor tissues and the amount of Lactobacillus sp. and Lachnospiraceae in mice stools, while there was no significant difference between LA and TC groups. These results provide a promising regimen to enhance the therapeutic effect in a dietary supplement manner.
Astaxanthin suppresses the metastasis of colon cancer by inhibiting the MYC-mediated downregulation of microRNA-29a-3p and microRNA-200a
We demonstrated that AXT increases miR-29a-3p and miR-200a expression, and thereby suppresses the expression of MMP2 and ZEB1, respectively. As a result, AXT represses the epithelial-mesenchymal transition (EMT) of CRC cells. Through the mechanistic study, we identified that AXT shows anti-metastatic activity through the transcriptional repression of MYC transcription factor. Finally, we also confirmed that AXT suppresses the in vivo metastatic capacity of colon cancer cell using mouse model. Collectively, we uncovered the novel function of AXT in the inhibition of EMT and invadopodia formation, implicating the novel therapeutic potential for AXT in metastatic CRC patients.
12. Bakterielle Infektionen
Astaxanthin-Mediated Bacterial Lethality: Evidence from Oxidative Stress Contribution and Molecular Dynamics Simulation
Put together, findings from this study underscored the nature and mechanism of antibacterial action of astaxanthin that could suggest practical approaches in enhancing our current knowledge of antibacterial arsenal and aid in the novel development of alternative natural topo2A inhibitor.
Astaxanthin prevents and reverses diet-induced insulin resistance and steatohepatitis in mice: A comparison with vitamin E
Importantly, astaxanthin reversed insulin resistance, as well as hepatic inflammation and fibrosis, in pre-existing NASH. Overall, astaxanthin was more effective at both preventing and treating NASH compared with vitamin E in mice. Furthermore, astaxanthin improved hepatic steatosis and tended to ameliorate the progression of NASH in biopsy-proven human subjects. These results suggest that astaxanthin might be a novel and promising treatment for NASH.
The Beneficial Effects of Astaxanthin on Glucose Metabolism and Modified Low-Density Lipoprotein in Healthy Volunteers and Subjects with Prediabetes
Conclusions: our results suggest that ASTX may have preventive effects against diabetes and atherosclerosis and may be a novel complementary treatment option for the prevention of diabetes in healthy volunteers, including subjects with prediabetes, without adverse effects.
Astaxanthin attenuates pulmonary fibrosis through lncITPF and mitochondria‐mediated signal pathways
In this study, lncITPF acting as the therapeutic target of astaxanthin was explored in depth. The findings elucidated that astaxanthin blocks the activated fibroblast proliferation and migration through lncITPF and mitochondria‐mediated signal pathways to alleviate pulmonary fibrogenesis.
Oral Astaxanthin Supplementation Prevents Peritoneal Fibrosis in Rats
Peritoneal thickness was significantly suppressed by AST supplementation. Astaxanthin diminished the number of CD68-, 8-hydroxy-2′-deoxyguanosine (8-OHdG)-, and monocyte chemoattractant protein-1 (MCP-1)-positive cells. Type 3 collagen, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and MCP-1 mRNA expression was significantly lower in Group 3 than in Group 1. Increased transforming growth factor-β (TGF-β) and Snail mRNA expression, vascular density, and the number of α-smooth muscle actin (α-SMA)-positive cells were also decreased in Group 3.
15. Degenerative Augenkrankheiten
Clinical Applications of Astaxanthin in the Treatment of Ocular Diseases: Emerging Insights
The efficacy of this carotenoid in the setting of retinal diseases, ocular surface disorders, uveitis, cataract and asthenopia is reported in numerous animal and human studies, which highlight its ability of modulating several metabolic pathways, subsequently restoring the cellular homeostatic balance. To maximize its multitarget therapeutic effects, further long-term clinical trials are warranted in order to define appropriate dosage, route of administration and exact composition of the final product.
Effects of 3-Month Astaxanthin Supplementation on Cardiac Function in Heart Failure Patients with Left Ventricular Systolic Dysfunction-A Pilot Study
In this study, following 3-month astaxanthin supplementation, suppressed oxidative stress and improved cardiac contractility and exercise tolerance were observed in HF patients with LV systolic dysfunction. Correlation between suppression of oxidative stress and improvement of cardiac contractility suggests that suppression of oxidative stress by astaxanthin supplementation had therapeutic potential to improve cardiac functioning.
17. Kognitive Schwäche
Effects of Composite Supplement Containing Astaxanthin and Sesamin on Cognitive Functions in People with Mild Cognitive Impairment: A Randomized, Double-Blind, Placebo-Controlled Trial
The CNSVS test revealed significant improvements in psychomotor speed and processing speed in the AS group compared with the placebo group, suggesting that the daily supplementation of AS improved cognitive functions related to the ability to comprehend, and perform complex tasks quickly and accurately. Our results provide support for the use of AS as a dietary supplementation for improving cognitive functions.
Astaxanthin Protects PC12 Cells against Homocysteine- and Glutamate-Induced Neurotoxicity
Using PC12 cell model, we showed that Glu and Hcy provoked a huge amount of reactive oxygen species (ROS) production, causing mitochondrial damage at EC50 20 and 10 mm, respectively. The mechanisms of action include: (1) increasing calcium influx; (2) producing ROS; (3) initiating lipid peroxidation; (4) causing imbalance of the Bcl-2/Bax homeostasis; and (5) activating cascade of caspases involving caspases 12 and 3. Conclusively, the damages caused by Glu and Hcy to PC12 cells can be alleviated by the potent antioxidant ATX.
In Vivo Effects of Free Form Astaxanthin Powder on Anti-Oxidation and Lipid Metabolism with High-Cholesterol Diet
Taken together, our results suggested that the appropriate addition of FFAP into high cholesterol diets increases liver anti-oxidative activity and reduces the concentration of lipid peroxidase and therefore, it may be beneficial as a material in developing healthy food.
Suppression Effect of Astaxanthin on Osteoclast Formation In Vitro and Bone Loss In Vivo
The administration of AST (5, 10 mg/kg) for 6 weeks suppressed the enhancement of serum calcium, inorganic phosphorus, alkaline phosphatase, total cholesterol, and tartrate-resistant acid phosphatase (TRAP) activity. The bone mineral density (BMD) and bone microarchitecture of the trabecular bone in the tibia and femur were recovered by AST exposure. Moreover, in the in vitro experiment, we demonstrated that AST inhibits osteoclast formation through the expression of the nuclear factor of activated T cells (NFAT) c1, dendritic cell-specific transmembrane protein (DC-STAMP), TRAP, and cathepsin K without any cytotoxic effects on bone marrow-derived macrophages (BMMs). Therefore, we suggest that AST may have therapeutic potential for the treatment of postmenopausal osteoporosis.
Astaxanthin-Rich Algal Meal and Vitamin C Inhibit Helicobacter pylori Infection in BALB/cA Mice
Mice treated with astaxanthin-rich algal meal or vitamin C showed significantly lower colonization levels and lower inflammation scores than those of untreated or control-meal-treated animals at 1 day and 10 days after the cessation of treatment. Lipid peroxidation was significantly decreased in mice treated with the astaxanthin-rich algal meal and vitamin C compared with that of animals not treated or treated with the control meal. Both astaxanthin-rich algal meal and vitamin C showed an inhibitory effect on H. pylori growth in vitro. In conclusion, antioxidants may be a new strategy for treating H. pylori infection in humans.
The Protective Effects of Astaxanthin on the OVA-Induced Asthma Mice Model
In conclusion, all of the data in this experiment indicated that astaxanthin has a protective effect against OVA-induced allergic asthma mice. The exposure of the mice to astaxanthin attenuated their airway inflammation and reduced the levels of IgE and IgG1. In addition, astaxanthin can regulate the Th1/Th2 imbalance by inhibiting the release of Th2 cytokines (IL-4 and IL-5) or increasing the release of Th1 cytokines (IFN-γ). Moreover, astaxanthin effectively suppressed AHR, the infiltration of inflammatory cells in the lung, mucus hypersecretion, lung fibrosis, and the expression of caspase-1 and caspase-3. Therefore, astaxanthin could be a promising protective agent for asthma patients.
Anti-Hyperuricemic Effects of Astaxanthin by Regulating Xanthine Oxidase, Adenosine Deaminase and Urate Transporters in Rats
These results indicated that the AST promoted UA excretion by regulating the urate transport proteins, and thus alleviated HUA. This study suggested that the AST could serve as an effective alternative to traditional medicinal drugs for the prevention of fructose-induced HUA.
Astaxanthin protects against osteoarthritis via Nrf2: a guardian of cartilage homeostasis
Ast attenuated ECM degradation of OA chondrocytes through the Nrf2 signaling, and ameliorated the IL-1β-induced inflammatory response and ECM degradation via blockade of MAPK signaling. Additionally, Ast alleviated TNF-α-induced ECM degradation and chondrocyte apoptosis by inhibiting the NF-κB signaling, suppressed TBHP-induced oxidative stress, and subsequently reduced chondrocyte apoptosis. In vitro results were finally corroborated in vivo by demonstrating that Ast attenuates the severity of cartilage destruction in a mouse model of OA.
Efficacy of Astaxanthin for the Treatment of Atopic Dermatitis in a Murine Model
When compared with vehicle-treated group, the administration of AST significantly reduced the clinical skin severity score. In addition, the spontaneous scratching in AD model mice was reduced by AST administration. Moreover, the serum IgE level was markedly decreased by the oral administration of AST compared to that in vehicle-treated mice. The number of eosinophils, total and degranulated mast cells all significantly decreased in the skin of AST-treated mice compared with vehicle-treated mice. The mRNA and protein levels of eotaxin, MIF, IL-4, IL-5 and L-histidine decarboxylase were significantly decreased in the skin of AST-treated mice compared with vehicle-treated mice. These results suggest that AST improves the dermatitis and pruritus in AD via the regulation of the inflammatory effects and the expression of inflammatory cytokines.
In Anbetracht der gesundheitlichen Vorteile, die Astaxanthin aufgrund seiner biologischen Aktivität verleiht, wie bereits erwähnt, ist es im Nahrungsnetz weit verbreitet [ 56 ]. Es wurde festgestellt, dass die breite Palette an Bioaktivitäten, die Astaxanthin aus Garnelen-Nebenprodukten besitzt, sowohl in vitro als auch in vivo gesundheitliche Vorteile aufweist [ 126 , 127 ]. Astaxanthin reduzierte die Freisetzung von Interleukinen, die Bildung von Cyclooxygenase-2 und Stickstoffmonoxid und die durch Radioaktivität induzierten DNA-Schäden sowie verbesserte entzündungsbedingte Signalwege [ 110 , 128 , 129 , 130 , 131 , 132 , 133 , 134]. Es wurde festgestellt, dass es einen gesunden Zustand verleiht, indem es oxidativen Stress reduziert, Singulett-Sauerstoff neutralisiert, freie Radikale abfängt, die Lipidperoxidation hemmt und die Immunität und Muskelgesundheit verbessert [ 5 , 7 , 89 , 135 , 136 , 137 ]. Mehrere Studien haben auch die Fähigkeit von Astaxanthin aus Garnelen gezeigt, Fettleibigkeit, Bluthochdruck, Hyperlipidämie und Herzbeschwerden zu reduzieren [ 138 , 139 , 140 , 141 ]. Diese Eigenschaften wurden seinen entzündungshemmenden Eigenschaften und der Verringerung von oxidativem Stress im Glukose- und Lipidstoffwechsel zugeschrieben [ 58 , 142 ]., 143 ]. Die Kontrolle des Blutdrucks durch Astaxanthin wurde durch seine Fähigkeit erklärt, oxidativen Stress und Vasokonstriktion zu reduzieren [ 7 , 141 , 144 , 145 , 146 ]. Astaxanthin aus natürlichen Quellen erhöhte die Ausdauer, verbesserte die Stressresistenz und beugte Entzündungen und Geschwüren vor [ 145 , 147 ].
Eine der wichtigsten physiologischen Aktivitäten von AX, die stark mit seiner antioxidativen Aktivität verbunden ist, ist seine entzündungshemmende Aktivität als Reaktion auf Entzündungen, die durch ROS-induzierte oxidative Schäden ausgelöst werden. Zahlreiche Studien haben gezeigt, dass AX die Signalübertragung des kanonischen Nuklearfaktors Kappa B (NFκB) als Reaktion auf oxidativen Stress über die Hemmung der IKK-Oxidation hemmt, unabhängig von der Quelle von ROS, Zelltypen oder Organen [ 31 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68]. Infolgedessen unterdrückte AX die NFκB-vermittelte Genexpression von entzündungsfördernden Zytokinen wie IL-1β, IL-6, IL-8, iNOS oder TNFα und hemmte so die Entstehung von Entzündungen. Es wird berichtet, dass AX die Phosphorylierung und Kerntranslokation von STAT3 im 7,12-Dimethylbenz[a]anthracen (DMBA)-induzierten Karzinogenesemodell der Hamster-Bukkaltasche (HBP) hemmt [ 69 ]. Daher ist es wahrscheinlich, dass AX hemmend auf den JAK/STAT-Signalweg wirken kann, der ein Entzündungssignalweg von Zytokinen wie IL-6 ist, obwohl es kaum Hinweise darauf gibt, dass er in allen Zellen auf die gleiche Weise wirkt (Figur 3).