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Astaxanthin is an important immunoactive adjuvant. The present study was conducted to evaluate the effect of glucocorticoid receptor (GR) in astaxanthin alleviates LPS-induced immune stress in Channa argus lymphocyte. After astaxanthin or PDTC treatment, lymphocytes exposed to 10 μg/mL LPS for 24 h, showed significantly decreased NF-κB p65, TNF-α, IL-1β, IL-6, IL-8, NO, NOS, caspase-3, caspase-8 and caspase-9 levels. Upon LPS stimulation, astaxanthin significantly upregulated GR, HSP70 and HSP90 gene expression, in response to inflammatory responses. Treatment with GR inhibitors (RU486) or astaxanthin and 10 μg/ml LPS exposure, showed that RU486 significantly inhibited GR phosphorylation and blocked astaxanthin alleviated LPS-induced NF-κB pathway activation. Meanwhile, RU486 interfered with the anti-inflammatory and increased the inflammatory and apoptotic factors expression levels under LPS stimulation. Collectively, GR plays major role in astaxanthin alleviates LPS-induced immune stress in Channa argus lymphocyte. • Glucocorticoid receptor (GR) interacts with NF-κB to inhibit the inflammatory response in lymphocytes. • Astaxanthin inhibits NF-κB activation by phosphorylation of glucocorticoid receptor (GR) in lymphocytes. • Under the inhibition of GR activity, anti-inflammatory activity of astaxxanthin was attenuated in lymphocytes. [ABSTRACT FROM AUTHOR]

The effects of astaxanthin supplementationon the growth, innate immunity and antioxidant defence system of loach (Paramisgurnus dabryanus) were investigated in this study. A total of 450 fish (initial average weights of 3.00 ± 0.10 g) were fed five diets with graded levels of astaxanthin (0.00, 50.00, 100.00, 150.00 and 200.00 mg/kg) for 56 days. The results showed that astaxanthin supplementation significantly stimulated the growth (FBW, WG, FER, HSI), innate immunity (AKP activity in the hepatopancreas, intestinal tract, muscle and skin and LZM activity in the hepatopancreas, intestinal tract and skin), antioxidant ability (T‐SOD, GSH‐PX and CAT activities and T‐AOC, GSH and MDA contents in the hepatopancreas, intestinal tract, muscle and skin) of loach. Moreover, dietary astaxanthin supplementation significantly up‐regulated the relative mRNA levels of Nrf2 and Maf, and down‐regulated the relative mRNA level of Keap1 in the hepatopancreas when the supplementation levels of astaxanthin were 50–200 mg/kg. In conclusion, the diets with 100–151.06 mg/kg astaxanthin supplementation were optimal for loach, which based on the growth, immunity and antioxidant‐related indicators, and the astaxanthin supplementation regulated the antioxidant ability partially referring to Keap1‐Nrf2 signallings. [ABSTRACT FROM AUTHOR]

The present study was conducted to evaluate the effects of astaxanthin (AST) against lipopolysaccharide (LPS)‐induced lymphocyte viability, ultrastructural lesions, apoptosis, oxidative stress and inflammatory responses in Channa argus. Lymphocytes exposed to more than 10 μg/ml LPS alone for 24 hr showed significantly decreased cell viability, elevated nitric oxide (NO) and malondialdehyde (MDA), lactate dehydrogenase (LDH) contents, and increased nuclear factor κB p65 (NF‐κB p65), myeloid differential protein‐88 (MyD88), tumour necrosis factor‐α (TNF‐α), interleukin‐1β (IL‐1β), interleukin‐8 (IL‐8), caspase‐3, caspase‐8 and caspase‐9 gene expression. LPS at a concentration of 10 μg/ml could induce oxidative stress and inflammatory responses in lymphocytes. The activities of antioxidant enzymes (catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD)) were significantly decreased after exposure to 10 μg/ml LPS. Besides, AST strikingly antagonized the LPS‐induced negative effects. AST significantly increased the expression of HSP70, HSP90, IκB‐α, and glucocorticoid receptor (GR) and decreased inflammatory responses. Further study showed that AST can activate GR signalling pathway and inhibit p65 phosphorylation. In addition, AST attenuated LPS‐induced apoptosis, mitochondrial swelling, degeneration and vacuolization. Collectively, these findings suggest that AST has protective roles in LPS‐induced cell damage via modulating GR activation in C. argus lymphocytes. [ABSTRACT FROM AUTHOR]

The present study investigated the effects of dietary astaxanthin on the growth, blood biochemical, antioxidant, immune and inflammatory response in lipopolysaccharide‐challenged Channa argus. A total of 0, 50, 100 and 200 mg/kg of astaxanthin were added to the basal die for 56 days. After the feeding experiment, each group was subjected to a lipopolysaccharide challenge (except for the Control group). The results showed that adding astaxanthin to the diet can significantly increase the weight gain and specific growth rate and decrease the feed conversion ratio of C. argus; the highest weight gain, specific growth rate and minimum feed conversion ratio occurred in the 100 mg/kg group. Furthermore, dietary astaxanthin supplementation can alleviate the negative effects of lipopolysaccharides by increasing the levels of alkaline phosphatase, lysozyme, complement 3, complement 4, total serum protein, albumin, globulin, superoxide dismutase, catalase and glutathione peroxidase and decrease the serum cortisol, aspartate aminotransferase, alanine aminotransferase, glutathione peroxidase, and malondialdehyde. Dietary astaxanthin supplementation also can decrease the relative expression of inflammatory genes (nuclear factor κB, interleukin‐1, interleukin‐8 and tumour necrosis factor‐α) in the liver, spleen, kidney and intestine. To summarise, dietary astaxanthin addition can improve the growth performance and attenuate the negative effects of lipopolysaccharide challenge in C. argus. The optimal amount of astaxanthin is 100 mg/kg. [ABSTRACT FROM AUTHOR]

Abstract The present study was conducted to evaluate the protective effects of astaxanthin against lipopolysaccharide (LPS)-induced inflammatory responses in Channa argus in vivo and ex vivo. Primary hepatocytes were exposed to different concentrations of LPS for 24 h to induce an inflammatory response, and the protective effects of astaxanthin against LPS-induced inflammation were studied ex vivo and in vivo. Hepatocytes exposed to LPS (5–20 μg mL−1) alone for 24 h resulted in a significant increase in lactate dehydrogenase release (LDH), Nitric oxide (NO) production and Malondialdehyde (MDA) content, 10 μg mL−1 LPS could induced inflammatory response in hepatocytes. Gene expression of TLR4, NFkBp65, MAPKp38, TNF-α, IL-6 and IL-1β mRNA expression were also enhanced ex vivo (p < 0.05). In vivo test demonstrated that pretreatment with astaxanthin prevented the LPS-induced upregulation of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β. Besides, astaxanthin blocked the expression of Toll-like receptor 4 (TLR4) and then suppressed the phosphorylation of nuclear transcription factor-kappa B (NF-κB) p65 and degradation inhibitor of NF-κBα (IκBα). Further study showed that astaxanthin could suppress the phosphorylation of p38, extracellular signal-regulated kinase (ERK) and c-jun NH2-terminal kinase (JNK) in mitogen-activated protein kinase (MAPK) signal pathway. In conclusion, our results suggest that astaxanthin played an anti-inflammatory role by regulating TLR4 and the NF-κB and MAPK signaling pathways in C. argus. Highlights • We established LPS induced inflammatory response model in Channa argus hepatocytes in vitro. • Astaxanthin prevented LPS-induced upregulation of pro-inflammatory cytokines and related gene expression. • Astaxanthin attenuates inflammatory responses by suppressing NF-κB and MAPK signaling pathways in Channa argus. [ABSTRACT FROM AUTHOR]

Selenium (Se) is the most common micronutrient and that becomes toxic when present at higher concentrations in aquatic environments. Astaxanthin (AST) has been documented to possess antioxidant and anti-inflammatory properties. The aim of this study was to explore the potential of dietary AST and Se exposure on oxidative stress, and inflammatory response in Channa argus. After acclimation, 540 fish were randomly distributed into nine groups housed in twenty-seven glass tanks. The fish were exposed for 8 weeks to waterborne Se at 0, 100 and 200 μg L−1 or dietary AST at 0, 50 and 100 mg kg−1. The results shown that Se accumulation in the kidney, liver, spleen, intestine and gill were significantly increased following Se exposure, dietary 50 and 100 mg kg−1 AST supplementation decreased the accumulation of Se in the kidney, liver, spleen, and intestine. In addition, AST supplementation can decrease oxidative stress and inflammatory response in the liver and spleen following exposure to waterborne Se. These results indicate that AST has the potential to alleviate the effects of Se toxicity in C. argus. • Exposure to waterborne Se induced significant bioaccumulation in specific tissues. • The profile of Se accumulation: kidney ≈ liver > spleen > intestine > gill > muscle. • Oxidative stress and inflammatory response were affected following exposure to waterborne Se. • Astaxanthin supplementation effectively attenuated Se-induced toxicity. [ABSTRACT FROM AUTHOR]

The present study was conducted to evaluate the effects of dietary astaxanthin (AX) supplementation on lipopolysaccharide (LPS)-induced oxidative stress, immune responses and glucocorticoid receptor (GR)-related gene expression in Channa argus. A basal diet was supplemented with AX at 0, 50, 100 and 200 mg/kg feed for 56 days. The results showed that after LPS challenge, superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GPx), glutathione reductase (GSH-Rt), lysozyme (LZM), complement 3 (C3), complement 4 (C4) were significantly reduced (P <.05), while malondialdehyde (MDA), interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α) levels were significantly increased (P <.05) in liver, spleen, kidney and intestine. Dietary AX supplementation could alleviate LPS induced above changes in C. argus. Dietary AX supplementation significantly increased (P <.05) gene expression levels including heat shock protein 70 (HSP70), heat shock protein 90 (HSP90) and glucocorticoid receptor (GR) after LPS challenge. The protective effects of AX on LPS-induced oxidative damage is associated with promoting the levels of antioxidant enzymes and immune parameters. In addition, AX can attenuate LPS-induced inflammation response by up-regulating GR-related gene expression in C. argus. • Astaxanthin conferred protective effects against LPS-induced oxidative stress. • Astaxanthin improved immune responses in Channa argus. • Astaxanthin regulated GR-related genes expression in Channa argus. [ABSTRACT FROM AUTHOR]