Astaxanthin

Int Immunopharmacol. 2014 Mar;19(1):174-7.

Astaxanthin reduces matrix metalloproteinase expression in human chondrocytes.[Pubmed: 24480614]

Astaxanthin is a red carotenoid pigment which exerts multiple biological activities. However, little is known about the effects of Astaxanthin on matrix metalloproteinases (MMPs) in OA.
METHODS AND RESULTS:
The present study investigated the effects of Astaxanthin on MMPs in human chondrocytes. Human chondrocytes were pretreated with Astaxanthin at 1, 10 or 50μM, then, cells were stimulated with IL-1β (10ng/ml) for 24h. MMP-1, MMP-3 and MMP-13 were observed. We found that Astaxanthin reduced the expression of MMP-1, MMP-3 and MMP-13 as well as the phosphorylation of two mitogen-activated protein kinases (MAPK) (p38 and ERK1/2) in IL-1β-stimulated chondrocytes. Astaxanthin also blocked the IκB-α degradation.
CONCLUSIONS:
These results suggest that Astaxanthin may be beneficial in the treatment of OA.

AAPS J . 2017 Mar;19(2):421-430.

Epigenetic CpG Methylation of the Promoter and Reactivation of the Expression of GSTP1 by Astaxanthin in Human Prostate LNCaP Cells[Pubmed: 27913949]

Abstract Astaxanthin (AST), a red dietary carotenoid, has synergistic antioxidant effects with polyunsaturated fatty acids at low concentrations via Nuclear factor (erythroid-derived 2)-like 2 (NFE2L2 or Nrf2)/antioxidant response element (ARE) signaling. In addition, chromatin remodeling and DNA methylation-based gene silencing represent a common mechanism in prostate carcinogenesis and tumor progression from normal cells to pre-initiated cells and ultimately to invasive carcinoma. Therefore, the control of epigenetic modification and the transcriptional/translational control of the activation of Nrf2 and Nrf2-target genes, including glutathione S-transferases (GSTs), appear to be an important mechanism that protects cells against injuries from oxidative stress and cancer development. In this study, we aim to investigate the role of AST in reactivating the expression of Nrf2 and GSTP1 through epigenetic modification in human prostate LNCaP cells. Treatment with AST in human LNCaP cells reduced the methylation of 21 CpG sites of the GSTP1 CpG island but did not affect the three CpG sites of the Nrf2 promoter region. AST induced the mRNA expression and protein expression of both Nrf2 and GSTP1. It also increased the mRNA expression of NQO1 in sh-mock LNCaP cells but not in sh-SETD7 LNCaP cells. Furthermore, AST reduced the protein expression of DNMT3b and significantly inhibited DNMT and HDAC activities in vitro. Taken together, these results suggest that AST decreased the methylation status of the GSTP1, and these epigenetic modifying effects may originate from the decreasing activities of epigenetic modification enzymes, contributing to the overall beneficial health effects of AST. Keywords: DNA methylation; GSTP1; Astaxanthin; epigenetics; prostate cancer.

Metab Brain Dis. 2015 Jun 27.

The antioxidant effect of astaxanthin is higher in young mice than aged: a region specific study on brain.[Pubmed: 26116165]

Astaxanthin is a potential antioxidant which shows neuroprotective property. We aimed to investigate the age-dependent and region-specific antioxidant effects of Astaxanthin in mice brain.
METHODS AND RESULTS:
Animals were divided into 4 groups; treatment young (3 months, n = 6) (AY), treatment old (16 months, n = 6) (AO), placebo young (3 months, n = 6) (PY) and placebo old (16 months, n = 6) (PO) groups. Treatment group was given Astaxanthin (2 mg/kg/day, body weight), and placebo group was given 100 μl of 0.9% normal saline orally to the healthy Swiss albino mice for 4 weeks. The level of non-enzymatic oxidative markers namely malondialdehyde (MDA); nitric oxide (NO); advanced protein oxidation product (APOP); glutathione (GSH) and the activity of enzymatic antioxidants i.e.; catalase (CAT) and superoxide dismutase (SOD) were determined from the isolated brain regions. Treatment with Astaxanthin significantly (p < 0.05) reduces the level of MDA, APOP, NO in the cortex, striatum, hypothalamus, hippocampus and cerebellum in both age groups. Astaxanthin markedly (p < 0.05) enhances the activity of CAT and SOD enzymes while improves the level of GSH in the brain. Overall, improvement of oxidative markers was significantly greater in the young group than the aged animal.
CONCLUSIONS:
In conclusion, we report that the activity of Astaxanthin is age-dependent, higher in young in compared to the aged brain.

Rev Biol Trop. 2014 Dec;62(4):1331-41.

The effect of astaxanthin on resistance of juvenile prawns Macrobrachium nipponense (Decapoda: Palaemonidae) to physical and chemical stress.[Pubmed: 25720170]

In recent years, the use of new scientific techniques has effectively improved aquaculture production processes. Astaxanthin has various properties in aquaculture and its antioxidant benefits have been closely related to stress resistance; besides, it is an essential factor for growth in many crustaceans and fish. The objective of this study was to evaluate the resistance of prawn (Macrobrachium nipponense) fed diets containing different amounts of Astaxanthin (AX) to the shock and stress of different physicochemical environments.
METHODS AND RESULTS:
A 70-day trial was conducted to evaluate the effect of supplementation of a source of Astaxanthin (Carophyll Pink, 10% Astaxanthin, w/w, Hoffman-La Roche, Switzerland) at various levels in the diet of M. nipponense juveniles. Four dry diets were prepared: AX0 without Astaxanthin, AX50 with 50 mg/kg, AX100 with 100 mg/kg, and AX150 with 150 mg/kg Astaxanthin. The feeding trial was conducted in a recirculation water system consisting of 12 fiberglass tanks (1000L) used for holding prawns. Three replicate aquaria were initially stocked with 36 org/m2 per tank. During the trial, prawns were maintained on a 12:12-h light:dark photoperiod with an ordinary incandescent lamp, and the water quality parameters were maintained as follows: water temperature, 25-26°C; salinity, 1 g/L; pH, 8.5-8.8; dissolved oxygen, 6.0-6.5 mg/L; and ammonia-nitrogen, 0.05 mg/L. Incorporation of AX, production output, and physiological condition were recorded after 10 weeks of feeding. At the end of the growing period, the prawns were exposed to thermal shock (0°C), ammonia (0.75 mg/L), and reduced oxygen (0.5 mg/L). The time to lethargy and the time to complete death of the prawns were recorded. The results showed that control prawns had the shortest time to lethargy and death compared with prawns subjected to the other treatments. The results of this study have shown that the amount of muscle tissue and gill carotenoids in prawn fed with an AX150 diet showed greater reduction than those exposed to other treatments. It is possible that higher levels of Astaxanthin in the body under oxygen reduction stress can be beneficial for prawns.
CONCLUSIONS:
These results suggest that male prawns showed lethargy earlier than females, and the percentage of carotenoid reduction in muscle and gill tissues was higher in males.

Neuropharmacology. 2014 Sep;84:13-8.

The protective effect of astaxanthin on fetal alcohol spectrum disorder in mice.[Pubmed: 24780381]

Astaxanthin is a strong antioxidant with the ability of reducing the markers of inflammation.
METHODS AND RESULTS:
To explore the protective effect of Astaxanthin on maternal ethanol induced embryonic deficiency, and to investigate the underlying mechanisms, we detected the morphology, expression of neural marker genes, oxidative stress indexes, and inflammatory factors in mice model of fetal alcohol spectrum disorder with or without Astaxanthin pretreatment. Our results showed that Astaxanthin blocked maternal ethanol induced retardation of embryonic growth, and the down-regulation of neural marker genes, Otx1 and Sox2. Moreover, Astaxanthin also reversed the increases of malondialdehyde (MDA), hydrogen peroxide (H2O2), and the decrease of glutathione peroxidase (GPx) in fetal alcohol spectrum disorder. In addition, maternal ethanol induced up-regulation of toll-like receptor 4 (TLR4), and the down-streaming myeloid differentiation factor 88 (MyD88), NF-κB, TNF-α, and IL-1β in embryos, and this was inhibited by Astaxanthin pretreatment.
CONCLUSIONS:
These results demonstrated a protective effect of Astaxanthin on fetal alcohol spectrum disorder, and suggested that oxidative stress and TLR4 signaling associated inflammatory reaction are involved in this process.

BJU Int. 2014 Sep;114(3):458-66.

Astaxanthin modulates osteopontin and transforming growth factor β1 expression levels in a rat model of nephrolithiasis: a comparison with citrate administration.[Pubmed: 24712822]

To evaluate the effect of Astaxanthin on renal angiotensin-I converting enzyme (ACE) levels, osteopontin (OPN) and transforming growth factor β1 (TGF-β1) expressions and the extent of crystal deposition in experimentally induced calcium oxalate kidney stone disease in a male Wistar rat model. To compare the efficacy of Astaxanthin treatment with a currently used treatment strategy (citrate administration) for kidney stones.
METHODS AND RESULTS:
The expression of OPN was assessed by immunohistochemistry. One step reverse transcriptase polymerase chain reaction followed by densitometry was used to assess renal OPN and TGF-β1 levels. Renal ACE levels were quantified by an enzyme-linked immunosorbent assay method. Crystal deposition in kidney was analysed by scanning electron microscopic (SEM)-energy-dispersive X-ray (EDX). The renal ACE levels and the expression of OPN and TGF-β1 were upregulated in the nephrolithiasis-induced rats. Astaxanthin treatment reduced renal ACE levels and the expression OPN and TGF-β1. SEM-EDX analysis showed that crystal deposition was reduced in the Astaxanthin-treated nephrolithiatic group. Astaxanthin treatment was more effective than citrate administration in the regulation of renal ACE levels, OPN and TGF-β1 expressions.
CONCLUSIONS:
Astaxanthin administration reduced renal calcium oxalate crystal deposition possibly by modulating the renal renin-angiotensin system (RAS), which reduced the expression of OPN and TGF-β1 levels. Astaxanthin administration was more effective than citrate treatment in reducing crystal deposition and down-regulating the expression of OPN and TGF-β1.