Effects Of Astaxanthin Research Articles

Effect of Astaxanthin on the Expression and Activity of Aquaporin-3 in Skin in an In-Vitro Study.

Astaxanthin (3,3′-dihydroxy-β,β-carotene-4,4′-dione) is a red lipophilic pigment with strong antioxidant action. Oral or topical administration of astaxanthin has been reported to improve skin function, including increasing skin moisture. In this study, we examined the mechanism by which astaxanthin improves skin function by focusing on the water channel aquaporin-3 (AQP3), which plays important roles in maintaining skin moisture and function. When astaxanthin was added to PHK16-0b or HaCaT cells, the mRNA expression level of AQP3 increased significantly in a concentration-dependent manner in both cell lines. The AQP3 protein expression level was also confirmed to increase when astaxanthin was added to HaCaT cells. Similarly, when astaxanthin was added to 3D human epidermis model EpiSkin, AQP3 expression increased. Furthermore, when glycerol and astaxanthin were simultaneously added to EpiSkin, glycerol permeability increased significantly compared with that observed for the addition of glycerol alone. We demonstrated that astaxanthin increases AQP3 expression in the skin and enhances AQP3 activity. This result suggests that the increased AQP3 expression in the skin is associated with the increase in skin moisture by astaxanthin. Thus, we consider astaxanthin useful for treating dry skin caused by decreased AQP3 due to factors such as diabetes mellitus and aging.

Astaxanthin alleviates spinal cord ischemia-reperfusion injury via activation of PI3K/Akt/GSK-3\u03b2 pathway in rats

BackgroundIschemia-reperfusion injury of the spinal cord (SCII) often leads to unalterable neurological deficits, which may be associated with apoptosis induced by oxidative stress and inflammation. Astaxanthin (AST) is a strong antioxidant and anti-inflammatory agent with multitarget neuroprotective effects. This study aimed to investigate the potential therapeutic effects of AST for SCII and the molecular mechanism.MethodsRat models of SCII with abdominal aortic occlusion for 40 min were carried out to investigate the effects of AST on the recovery of SCII. Tarlov’s scores were used to assess the neuronal function; HE and TUNEL staining were used to observe the pathological morphology of lesions. Neuron oxidative stress and inflammation were measured using commercial detection kits. Flow cytometry was conducted to assess the mitochondrial swelling degree. Besides, Western blot assay was used to detect the expression of PI3K/Akt/GSK-3β pathway-related proteins, as well as NOX2 and NLRP3 proteins.ResultsThe results demonstrated that AST pretreatment promoted the hind limb motor function recovery and alleviated the pathological damage induced by SCII. Moreover, AST significantly enhanced the antioxidative stress response and attenuated mitochondrial swelling. However, AST pretreatment hardly inhibited the levels of proinflammatory cytokines after SCII. Most importantly, AST activated p-Akt and p-GSK-3β expression levels. Meanwhile, cotreatment with LY294002 (a PI3K inhibitor) was found to abolish the above protective effects observed with the AST pretreatment.ConclusionOverall, these results suggest that AST pretreatment not only mitigates pathological tissue damage but also effectively improves neural functional recovery following SCII, primarily by alleviating oxidative stress but not inhibiting inflammation. A possible underlying molecular mechanism of AST may be mainly attributed to the activation of PI3K/Akt/GSK-3β pathway.

Anti-Migration and Invasion Effects of Astaxanthin against A172 Human Glioblastoma Cell Line.

Objectives:The study was to investigate anti-migration and invasion effects of astaxanthin (ATX), a natural carotenoid derivative distributed in marine environments, against A172 human glioblastoma cells. Materials and Methods:Cell viability after ATX treatment was measured by MTT assays. Tumor cell migration and invasion were observed by scratch and Boyden chamber assays, respectively. Expression of MMP-2 and activity of MMP-9 were observed by immunoblotting and gelatin zymography, respectively. Results:ATX up to 150 µM was not toxic to A172 cells at 48 h post-treatment. In contrast, ATX at 50 and 100 µM significantly decreased migration and invasion of A172 cells at 24 and 48 h post-treatment. Metastatic-reducing effect of ATX is associated with the reduction of MMP-2 and MMP-9 expressions in a dose-dependent manner. Conclusion: This finding indicated that ATX has anti-migration and invasion effects against human glioblastoma cells and might be applicable for the protection against metastasis of glioblastoma.

Effects of astaxanthin on the immune response and reproduction of Procambarus clarkii stressed with microcystin-leucine-arginine

The aim of this study was to evaluate the effects of the antioxidant astaxanthin on the immune response, growth, and reproduction of the crayfish Procambarus clarkii (Girard, 1852) stressed with the toxin microcystin-leucine-arginine (MC-LR). P. clarkii exposed to MC-LR were treated with one of four concentrations of dietary astaxanthin supplement (0, 2.5, 5, or 10 mg/g) for 36 consecutive days in tanks. In crayfish exposed to 0.05 mg/l MC-LR, activity levels of superoxide dismutase and alkaline phosphatase in the hepatopancreas significantly increased (P < 0.05) following dietary supplementation with 10 mg/g astaxanthin. The survival and fecundity of P. clarkii decreased significantly with exposure to 0.01 mg/l MC-LR, but astaxanthin supplementation significantly improved survival (P < 0.05). The average daily oxygen consumption rate of P. clarkii stressed with 0.01 mg/l MC-LR was significantly higher than that of unstressed P. clarkii (P < 0.05); astaxanthin supplementation did not significantly affect the average daily oxygen consumption rate of MC-LR-stressed P. clarkii. In conclusion, the antioxidant astaxanthin was found to be a suitable dietary supplement for P. clarkii as it improved immune activity and alleviated MC-LR-induced oxidative stress.

Comparison of Different Molecular Forms of Astaxanthin in Inhibiting Lipogenesis and its Mechanism.

Astaxanthin is a natural active substance with a plurality of biological activities, such as anti-oxidation, anti-inflammatory and anti-cardio-cerebrovascular diseases. However, there is less research on the effects of astaxanthin on obesity. Astaxanthin with different structural forms affect the corresponding biological activity. The study aimed to compare Astaxanthin-octanoic acid diester (C8-AST) and Free Astaxanthin (F-AST) to explore the effect on lipogenesis in vitro. 3T3-L1 preadipocytes were cultured under astaxanthin treatment. Cell proliferation and differentiation were evaluated by MTT assay and oil red O staining, respectively. The synthesis of metabolic mechanism of intracellular fatty acids and triglycerides was examined by qRT-PCR and Western blotting. C8-AST and F-AST had no effect on adipocyte proliferation at low concentration, but inhibited adipocyte differentiation. The treatment of astaxanthin could inhibit the expression of PPARγ, C/EBPα and SREBP-1c in adipocytes, up-regulate the expression of Wnt10b, LRP6, FZ in Wnt/ β-catenin signaling pathway and increase the β-catenin entry into nucleus, suggesting that the activation of Wnt/β-catenin signaling was involved in axtaxanthin-regulated lipogenesis. Notably, inhibition effect of lipogenesis on C8-AST was better than F-AST overall. At the cellular level, both two kinds of astaxanthins inhibit the synthesis of intracellular fatty acids and triglycerides. Notably, the inhibition effect of C8-AST is better than F-AST overall.

Neuroprotective effects of astaxanthin against oxygen and glucose deprivation damage via the PI3K/Akt/GSK3β/Nrf2 signalling pathway in vitro.

Astaxanthin (ATX), which is the most abundant flavonoid in propolis, has previously shown neuroprotective properties against cerebral ischaemia‐induced apoptosis. However, the mechanisms by which ATX mediates its therapeutic effects are unclear. At present, we explored the underlying mechanisms involved in the protective effects of ATX via the phosphoinositide 3‐kinase (PI3K)/Akt/glycogen synthase kinase 3 beta (GSK3β)/nuclear factor erythroid 2‐related factor 2 (Nrf2) signalling pathway in SH‐SY5Y cells. The PI3K/Akt inhibitor LY294002 and GSK3β inhibitor LiCl were employed in this study. Pre‐treatment with ATX for 24 hours significantly decreased the oxygen and glucose deprivation (OGD)‐induced viability loss, reduced the proportion of apoptosis and regulated OGD‐mediated reactive oxygen species (ROS) production. Furthermore, ATX suppressed OGD‐caused mitochondrial membrane potential and decomposition of caspase‐3 to cleaved caspase‐3, and heightened the B‐cell lymphoma 2 (Bcl‐2)/Bax ratio. PI3K/Akt/GSK3β/Nrf2 signalling pathway activation in SH‐SY5Y cells was verified by Western blot. ATX and LiCl treatment raised the protein levels of p‐Akt, p‐GSK3β, nucleus Nrf2 and haeme oxygenase 1 (HO‐1). However, these protein expression levels decreased by treatment of LY294002. The above in vitro data indicate that ATX can confer neuroprotection against OGD‐induced apoptosis via the PI3K/Akt/GSK3β/Nrf2 signalling pathway.

Astaxanthin inhibits the reduction of glycolysis during the activation of hepatic stellate cells

AimsHepatic stellate cells (HSCs) play an essential role in the development of liver fibrosis by producing extracellular matrix proteins, growth factors, and pro-inflammatory and pro-fibrogenic cytokines once activated. We previously demonstrated that astaxanthin (ASTX), a xanthophyll carotenoid, attenuates HSC activation. The objective of this study was to investigate whether there is a difference in glycolysis between quiescent and activated HSCs and the effect of ASTX on glycolysis during HSC activation. Materials and methodsMouse primary HSCs were activated for 7 days in the presence or absence of 25 μM of ASTX. Quiescent HSCs (qHSCs), 1 day after isolation, and activated HSCs (aHSCs) treated with/without ASTX were plated in a Seahorse XF24 cell culture microplate for Glycolysis Stress tests. Key findingsaHSCs had significantly lower glycolysis, but higher glycolytic capacity, maximum capacity of glycolysis, and non-glycolytic acidification than qHSCs. Importantly, ASTX markedly increased glycolysis during HSC activation with a concomitant increase in lactate formation and secretion. Compared with qHSCs, aHSCs had significantly lower expression of glucose transporter 1, the major glucose transporter in HSCs, and its transcription factor hypoxia-inducible factor 1α, which was markedly increased by ASTX in aHSCs. SignificanceOur data suggest that ASTX may prevent the activation of HSCs by altering glycolysis and the expression of genes involved in the pathways.

Effect of Astaxanthin on Activation of Autophagy and Inhibition of Apoptosis in Helicobacter pylori-Infected Gastric Epithelial Cell Line AGS.

Helicobacter pylori (H. pylori) infection leads to the massive apoptosis of the gastric epithelial cells, causing gastric ulcers, gastritis, and gastric adenocarcinoma. Autophagy is a cellular recycling process that plays important roles in cell death decisions and can protect cells by preventing apoptosis. Upon the induction of autophagy, the level of the autophagy substrate p62 is reduced and the autophagy-related ratio of microtubule-associated proteins 1A/1B light chain 3B (LC3B)-II/LC3B-I is heightened. AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) are involved in the regulation of autophagy. Astaxanthin (AST) is a potent anti-oxidant that plays anti-inflammatory and anti-cancer roles in various cells. In the present study, we examined whether AST inhibits H. pylori-induced apoptosis through AMPK-mediated autophagy in the human gastric epithelial cell line AGS (adenocarcinoma gastric) in vitro. In this study, H. pylori induced apoptosis. Compound C, an AMPK inhibitor, enhanced the H. pylori-induced apoptosis of AGS cells. In contrast, metformin, an AMPK activator, suppressed H. pylori-induced apoptosis, showing that AMPK activation inhibits H. pylori-induced apoptosis. AST inhibited H. pylori-induced apoptosis by increasing the phosphorylation of AMPK and decreasing the phosphorylation of RAC-alpha serine/threonine-protein kinase (Akt) and mTOR in H. pylori-stimulated cells. The number of LC3B puncta in H. pylori-stimulated cells increased with AST. These results suggest that AST suppresses the H. pylori-induced apoptosis of AGS cells by inducing autophagy through the activation of AMPK and the downregulation of its downstream target, mTOR. In conclusion, AST may inhibit gastric diseases associated with H. pylori infection by increasing autophagy through the activation of the AMPK pathway.

The effect of astaxanthin on inflammation in hyperosmolarity of experimental dry eye model in vitro and in vivo

Hyperosmolarity is pro-inflammatory stress to the ocular surface epithelium associated with dry eye disease (DED). Astaxanthin (AST) is a kind of carotene, which exists in seafood and plays important roles in the amelioration of inflammatory diseases like arteriosclerosis, inflammatory bowel disease, sepsis, rheumatoid arthritis, gastric inflammation, brain inflammatory diseases. The aim of this study was to characterize the protective effect and potential mechanism of AST on DED in vitro and in vivo. Mouse models and human corneal epithelial cell (HCEC) cultures were exposed to hyperosmotic saline solution (HOSS) in in vitro and in vivo experiments, respectively. Experimental subjects were first pretreated with AST, and then the effect of the compound was assessed with clinical evaluation, real-time PCR (RT-PCR), western blot and immunofluorescent staining. We further investigated the possible mechanism of AST in DED by pre-treating with phosphoinositide 3-kinase inhibitor (LY294002). The addition of AST significantly reduced the expression of High-mobility group box 1 (HMGB1), as well as significantly inhibited the increases of TNF-α, IL-1β in a dose-dependent manner, but promoted the expression of phospho-Akt (p-Akt). BALB/c mice in DE group pretreated with AST showed significantly decreased corneal fluorescein staining scores. Moreover, pretreatment with LY294002 could eliminate the effects of AST preconditioning on the decrease of HMGB1. Our study provides evidence that AST could ameliorate DED which may be related to the inhibition of HMGB1, TNF-α, IL-1β, while PI3K/Akt signaling pathway may be involved in the expression of HMGB1 and the protective effect of AST preconditioning.

Astaxanthin Supplementation Lowers Dietary Intake in Healthy Subjects

Astaxanthin, a potent antioxidant compound, is well recognized for its beneficial effects to protect from oxidative stress and free radicals. However, the effects of long period of use of astaxanthin on biological parameters, health indicators, and energy intake are still largely unknown. A total of 33 healthy participants aged 21–54 years with body mass index in the range of 18.50−24.90 kg/m2 were enrolled in this randomized controlled trial and were assigned into astaxanthin and placebo groups. The participants in the astaxanthin group received 4 mg of astaxanthin once daily for 12 consecutive weeks. Dietary intakes, as well as blood levels of astaxanthin and biological parameters, were investigated at baseline and week 12. The significant elevation of blood astaxanthin level in the astaxanthin group was notified at week 12. Regarding basic characteristics of blood biochemical parameters, results indicated that the fasting blood glucose, total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol were not significantly different between astaxanthin and placebo groups at week 12. Interestingly, the significant decrease in total energy and carbohydrate intakes of the participants in the astaxanthin group (P &lt; 0.05) was found after 12-week supplementation, compared to the baseline. The findings support the safety of long-term supplementation and reveal potential dietary intake lowering effect of astaxanthin in healthy individuals.

Effect of astaxanthin in extenders on sperm quality and functional variables of frozen-thawed boar semen

The aim of the study was to determine whether the presence of astaxanthin (ASX) protects boar spermatozoa against damage related to cryopreservation. Pooled ejaculates extended in Beltsville Thawing Solution (BTS) were used. Three experiments were conducted: 1) sperm samples were pre-incubated overnight (17 °C) with ASX (0, 0.5, 5, 15 μM) prior to freezing and then frozen using cooling and thawing extenders supplemented with ASX (0, 0.5, 5, 15 μM); 2) sperm samples were treated with ASX (0, 0.5, 5, 15 μM) only during overnight pre-incubation (17 °C) prior to cryopreservation; and 3) a thawing extender was supplemented with ASX (0, 0.5, 5, 15 μM). The groups were as follows: control (C; no treatment), ASX 1 (0.5 μM), ASX 2 (5 μM) and ASX 3 (15 μM). Total (TM) and progressive (PM) motility was analyzed using CASA, while sperm viability, reactive oxygen species generation, lipid peroxidation and apoptoticlike changes were analyzed using flow cytometry. Sperm variables were evaluated prior to freezing as well as 30 and 150 min after thawing. In Experiment 1, the values of TM and sperm viability post-thaw were less in the ASX 3 than C group. In Experiment 2, there was no effect of ASX on any of the sperm variables evaluated, while in Experiment 3, apoptotic-like changes were less in the ASX 1 than C group. In conclusion, there was a subtle beneficial effect on cryopreserved boar spermatozoa after addition of ASX to thawing media.

Astaxanthin Attenuates Hypertensive Vascular Remodeling by Protecting Vascular Smooth Muscle Cells from Oxidative Stress-Induced Mitochondrial Dysfunction.

Oxidative stress aggravates mitochondrial injuries and accelerates the proliferation of vascular smooth muscle cells (VSMCs), which are important mechanisms contributing to vascular remodeling in hypertension. We put forward the hypothesis that Astaxanthin (ATX), known to possess strong features of antioxidant, could attenuate vascular remodeling by inhibiting VSMC proliferation and improving mitochondrial function. The potential effects of ATX were tested on spontaneously hypertensive rats (SHRs) and cultured VSMCs that injured by angiotensin II (Ang II). The results showed that ATX lowered blood pressure, reduced aortic wall thickness and fibrosis, and decreased the level of reactive oxygen species (ROS) and H2O2 in tunica media. Moreover, ATX decreased the expression of proliferating cell nuclear antigen (PCNA) and ki67 in aortic VSMCs. In vitro, ATX mitigated VSMC proliferation and migration, decreased the level of cellular ROS, and balanced the activities of ROS-related enzymes including NADPH oxidase, xanthine oxidase, and superoxide dismutase (SOD). Besides, ATX mitigated Ca2+ overload, the overproduction of mitochondrial ROS (mtROS), mitochondrial dysfunction, mitochondrial fission, and Drp1 phosphorylation at Ser616. In addition, ATX enhanced mitophagy and mitochondrial biosynthesis by increasing the expression of PINK, parkin, mtDNA, mitochondrial transcription factor A (Tfam), and PGC-1α. The present study indicated that ATX could efficiently treat vascular remodeling through restraining VSMC proliferation and restoring mitochondrial function. Inhibiting mitochondrial fission by decreasing the phosphorylation of Drp1 and stimulating mitochondrial autophagy and biosynthesis via increasing the expression of PINK, parkin, Tfam, and PGC-1α may be part of its underlying mechanisms.

Metabolomic Analysis Reveals That the Mechanism of Astaxanthin Improves the Osteogenic Differentiation Potential in Bone Marrow Mesenchymal Stem Cells.

At present, little research has been done on the metabolic phenotype of the differentiation of mesenchymal stem cells (MSCs) into osteoblasts. In this study, the effect of astaxanthin on improving osteogenic differentiation potential of mesenchymal stem cells was studied by metabolomics. Results showed that L-methionine, L-tyrosine, and 2-hydroxycinnamic acid were upregulated in MSCs treated with astaxanthin, while L-lysine, L-pipecolic acid, L-histidine, L-arginine, D-fructose, and L-aspartic acid were downregulated in samples treated with astaxanthin. In addition, astaxanthin exhibited a significant dose-dependent relationship with these markers. Metabolic pathway enrichment analysis revealed that AST mainly regulated phenylalanine metabolism; phenylalanine, tyrosine, and tryptophan biosynthesis; and pantothenate and CoA biosynthesis during the process of osteogenic differentiation of MSCs. Furthermore, the staining results showed that astaxanthin could actively promote the osteogenic differentiation of mesenchymal stem cells. These findings clearly indicate that astaxanthin plays an important role in inducing osteogenic differentiation of mesenchymal stem cells. In addition, the changed metabolites can be used to monitor the differentiation process.

Effects of Astaxanthin on Body and Liver Weight of High-Fat Diet through Regulation of Peroxisome Proliferator-Activated Receptors (PPARs)

Effects of Astaxanthin on Body and Liver Weight of High-Fat Diet through Regulation of Peroxisome Proliferator-Activated Receptors (PPARs)

Protective Effect of Astaxanthin on Prenatal Bacterial Lipopolysaccharide Exposed Behavioral Deficits in Adult Mice

Background: Prenatal maternal lipopolysaccharide (LPS) exposure causes behavioral deficits in adulthood. LPS-exposure cause oxidative damage and cytokines production. In contrast, astaxanthin (Ast) is a carotenoid antioxidant that shows protective effects through its antioxidant capacity. Objectives: This study investigates the effect of prenatal treatment with astaxanthin on the behavioral deficit (including sexual, depressive, and anxiety-like behavior) caused by prenatal maternal LPS in adult male offspring. Methods: Pregnant mice were randomly divided into 4 groups: (1) control, (2) LPS: injecting with LPS (20 µg/kg, sc.) on gestation day 11, (3) Ast: receiving astaxanthin (4 mg/kg for 3 days, i.p.) on 11 - 13th gestation day, (4) LPS+Ast: injecting with LPS (20 µg/kg, sc.) on gestation day 11 and receiving astaxanthin (4 mg/kg for 3 days, i.p.) on 11 - 13th gestation day. Then in each group, 23 day old male offspring (3 and 12 male children from each mother and group, respectively) were separated from mothers and then the sexual, depressive and anxiety-like behaviors were examined in adult male mice. Results: Findings showed that prenatal LPS-exposed mice had more anxiety and spent less time in open arms of the elevated plus-maze test (P < 0.05). In addition, it decreased sexual behaviors, the amount of which was significant in the number of sniffing, following behaviors (P < 0.01). Also, there was no significant difference between different groups in the forced swimming test (P < 0.05). On the other hand, prenatal treatment with astaxanthin significantly elevated the percentage of open arm time and open arm entry, without altering in locomotor activity (P < 0.05). Also, it significantly increased sexual behavior in Ast and LPS+Ast groups (P < 0.01). Conclusions: The obtained results suggest that prenatal maternal exposure to LPS impaired several aspects of male sexual behavior and resulted in behavioral deficits in adulthood, while astaxanthin has an antianxiety effect and improves the deficits of sexual behavior presumably via its antioxidant property.

Efficacy of Astaxanthin Fed to Rainbow Trout (Oncorhynchus mykiss): Effect on Growth, Pigmentation and Blood Indices

In this study, the effect of astaxanthin on growth, pigmentation and blood factors were studied in rainbow trout weighted average (93±0.64 g) for 8 weeks. Two treatments and three replicates were employed as follows: Treatment A: fed with a commercial diet (control), treatment B: 41 mg/kg astaxanthin. All treatments were fed in hours 8, 12, 16, respectively. It should be considered that the feeding rate of biomass weight was examined after each took biometrics. Finally, blood samples were taken from the fish. The results revealed a significant difference between treatments in terms of weight and length (p&lt;0.05) and no significant difference (p&gt;0.05) in food intake and growth performance parameters, including FCR, SGR, GR, BWI%, and survival rate between treatments. In terms of pigmentation between experimental treatments, astaxanthin was created more change color than the control group. Results of blood factors showed that between WBC, RBC, Hb, HCT, Lymphocytes, Neutrophils, Monocytes and IgM were significant differences between treatments (p&lt;0.05). So we can conclude that 41mg/kg astaxanthin dietary, due to economy, would be proper diet in the feeding of rainbow trout propagation.

Astashine Capsules: A Natural Antioxidant, Anti-inflammatory Helps in Maintaining Lung Health and Minimizing SARS-CoV-2 effects in Covid-19 Infections

Astaxanthin is a naturally occurring carotenoid which is derived from the microalgae Haematococcuspluvialis. As well as being the most powerful antioxidant known to science, it also has potent anti-inflammatory properties. Naturalastaxanthin´s distinct advantage in comparison to other antioxidants, is its ability to span the entire lipid bilayer of the cell membrane, thus providing superior protection from the inside out. Natural astaxanthin has a strong ability to both balance and strengthen the immune system. This article reviews the current available scientific literature regarding the effect of astaxanthin from the algae Haematoccus pluvialis in Astashine capsules as a natural immune booster in COVID-19 infections.

虾青素在烟曲霉菌诱导的真菌性角膜炎中的抗炎作用

虾青素在烟曲霉菌诱导的真菌性角膜炎中的抗炎作用

The Effects of Astaxanthin on Proliferation and Differentiation of MG-63 Osteosarcoma Cells via Aryl Hydrocarbon Receptor (AhR) Pathway: A Comparison with AhR Endogenous Ligand

Background: Osteosarcoma (OS) is the most prevalent bone-related malignancy with a high mortality rate among children and adolescents. In the present study, first we explored the effects of astaxanthin (AST) on proliferation and differentiation of the MG-63 osteosarcoma cell line, and then compared its effects with AhR endogenous ligand (FICZ).Methods: Cell proliferation and cytotoxicity assay were performed using MTT. To identify possible mechanisms underlying AST-induced changes in osteogenic metabolism via the AHR pathway, we defined changes in CYP1A1, osteocalcin, osteopontin, type I collagen, and Runx2 gene expression using RT-PCR.Results: AST upregulated CYP1A1, osteocalcin, osteopontin, type I collagen, and Runx2 expression in trends of increasing its concentration. FICZ showed a biphasic effect on MG-63 cell proliferation. At high concentrations, it significantly decreased the cell viability, while at lower concentrations it was increased as compared to the control. Increasing FICZ concentrations from 1 nm to 1 μM, down-regulated the expression of Runx2, osteopontin, osteocalcin and collagen type 1 at the transcriptional levels. It seems that AST can augment the proliferation and differentiation of MG-63 via the AhR-dependent pathway, while FICZ suppresses the proliferation and differentiation of MG-63.Conclusion: We concluded that various AhR ligands show different behaviors in the modulation of MG-63 cells.

The Role of the Reactive Oxygen Species Scavenger Agent, Astaxanthin, in the Protection of Cisplatin-Treated Patients Against Hearing Loss.

Emerging evidence of significant hearing loss occurring shortly after cisplatin administration in cancer patients has stimulated research into the causes and treatment of this side effect. Although the aetiology of cisplatin-induced hearing loss (CIHL) remains unknown, an increasing body of research suggests that it is associated with excessive generation of intracellular reactive oxygen species (ROS) in the cochlea. Astaxanthin, a xanthophyll carotenoid, has powerful anti-oxidant, anti-inflammatory, and anti-apoptotic properties based on its unique cell membrane function, diverse biological activities, and ability to permeate the blood-brain barrier. In this review, we summarize the role of ROS in CIHL and the effect of astaxanthin on inhibiting ROS production. We focus on investigating the mechanism of action of astaxanthin in suppressing excessive production of ROS.