The Experts below are selected from a list of 315 Experts worldwide ranked by ideXlab platform
Xiaoqiu Zhou - One of the best experts on this subject based on the ideXlab platform.
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The toxic effects and potential mechanisms of deoxynivalenol on the structural integrity of Fish Gill: Oxidative damage, apoptosis and tight junctions disruption.
Toxicon, 2019Co-Authors: Chen Huang, Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Shengyao Kuang, Ling Tang, Xiaoqiu ZhouAbstract:Abstract Deoxynivalenol (DON) is a common mycotoxin existed in animal feed, and lead to significant economic loss due to its negative impacts on animal growth performance and animal health. The Gill is a primary mucosal immune organ in teleosts, and the structural integrity of the Gill is closely relevant with Fish healthy growth. Hence, this study assessed the influences of DON on the Gill structural integrity of juvenile grass carp, Ctenopharyngodan idella (initial average weight 12.17 ± 0.01 g), when offered with six different diets which contained various content of DON (27, 318, 636, 922, 1243 and 1515 μg/kg diet) for 60 days. Our research firstly systematically elaborated that DON caused histopathological lesions, oxidative injury, reduction of antioxidant ability, apoptosis as well as damages of tight junctions in Fish Gills. Comparing these data to the control, we found that DON at dose of more than 318 μg/kg diet led to oxidative injury, apoptosis and disruption of tight junctions in Fish Gill, which were likely to be relevant with Nrf2, JNK and MLCK signalling pathways, respectively. It was worth noting that DON was not found to affect the gene expressions of Keap1b (rather than Keap1a), claudin-b, claudin-3c and claudin-15b (not claudin-15a) in Fish Gills. Furthermore, based on MDA and T-AOC activities in the Gill, the maximum permissible levels of DON were evaluated to be 375.60 as well as 412.91 μg/kg diet in grass carp, respectively.
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Gill structural integrity changes in Fish deficient or excessive in dietary isoleucine towards the modulation of tight junction protein inflammation apoptosis and antioxidant defense via nf κb tor and nrf2 signaling pathways
Fish & Shellfish Immunology, 2017Co-Authors: Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Shengyao Kuang, Ling Tang, Yongan Zhang, Xiaoqiu Zhou, Wuneng TangAbstract:This study firstly aimed to test the impact of dietary isoleucine (Ile) on tight junction protein, inflammation, apoptosis, antioxidant defense and related signaling molecule gene expression in the Gill of Fish. Young grass carp (Ctenopharyngodon idella) (weighing 256.8 ± 3.5 g) were fed six diets containing graded levels of Ile, namely, 3.8, 6.6, 9.3, 12.5, 15.2 and 18.5 g/kg diet for 8 weeks. The results firstly revealed that Ile deficiency down-regulated the mRNA expressions of claudin-3, claudin-b, claudin-c, occludin and zonula occludens-1 (ZO-1) and up-regulated the mRNA expression of claudin-12, which led to the intercellular structure damage of Fish Gill. These effects were partially ascribed to the up-regulation of pro-inflammatory cytokines [interleukin 1β (IL-1β), interleukin 8 (IL-8) and tumor necrosis factor-α (TNF-α)] mRNA expressions that referring to up-regulated nuclear factor κB P65 (NF-κB P65) mRNA expression and down-regulated inhibitor factor κBα (IκBα) mRNA expression, and the down-regulation of anti-inflammatory cytokines [interleukin 10 (IL-10) and transforming growth factor β1 (TGF-β1)] mRNA expressions that referring to the down-regulated TOR and S6K1 mRNA expression. Interestingly, no change in claudin 15 mRNA level was observed among every treatment. At the same time, the results firstly indicated that Ile deficiency also resulted in the cellular structure damage of Fish Gill: (1) DNA fragmentation partially due to the up-regulation of caspase-3, caspase-8 and caspase-9 mRNA expression; (2) increase in protein carbonyl (PC), malondialdehyde (MDA) and ROS contents, which may be partially attributed to the impaired antioxidant defense [indicated by decreased glutathione (GSH) level and depressed anti-superoxide anion (ASA), anti-hydroxyl radical (a-HR), copper/zinc superoxide dismutase (Cu/Zn-SOD), catalase (CAT) and glutathione peroxidase (GPx) activities] that referring to the down-regulation of corresponding antioxidant enzyme mRNA expressions and the related signaling molecules Nrf2 mRNA expression. Ile excess caused similar negative effects that observed in Ile-deficient group, whereas these negative effects were reversed with appropriate Ile supplementation. In conclusion, our results indicated that Ile deficiency or excess disrupted the structural integrity of Fish Gill, partially due to the trigger of apoptosis, the impairment of antioxidant defense, and the regulation of tight junction protein, inflammatory cytokines, apoptosis-related, antioxidant enzymes and related signaling molecules mRNA expressions in the Fish Gill.
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changes in barrier health status of the Gill for grass carp ctenopharyngodon idella during valine deficiency regulation of tight junction protein transcript antioxidant status and apoptosis related gene expression
Fish & Shellfish Immunology, 2015Co-Authors: Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Shengyao Kuang, Ling Tang, Yongan Zhang, Xiaoqiu ZhouAbstract:This study investigated the effects of dietary valine on tight junction protein transcription, antioxidant status and apoptosis on grass carp Gills (Ctenopharyngodon idella). Fish were fed six different experimental diets containing graded levels of valine (4.3, 8.0, 10.6, 13.1, 16.7, 19.1 g/kg). The results indicated that valine deficiency decreased Claudin b, Claudin 3, Occludin and ZO-1 transcription and increased Claudin 15 expression in the Fish Gill (P 0.05). Valine deficiency also disrupted antioxidant status in the Gill by decreasing anti-superoxide radicals and hydroxyl radical capacity, glutathione contents and the activities and mRNA levels of Cu/Zn superoxide dismutase (SOD1), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST) (P < 0.05). These results may be ascribed to the down-regulation of NF-E2-related factor 2 (Nrf2), target of rapamycin (TOR) and ribosomal protein S6 kinase 1 (S6K1) and the up-regulation of Kelch-like-ECH-associated protein 1 (Keap1) (P < 0.05). Additionally, valine deficiency induced DNA fragmentation via the up-regulation of Caspase 3, Caspase 8 and Caspase 9 expressions (P < 0.05). These results may be ascribed to the improvement in ROS levels in the Fish Gill (P < 0.05). Taken together, the results showed that valine deficiency impaired the structural integrity of Fish Gill by disrupted Fish antioxidant defenses and regulating the expression of tight junction protein, cytokines, antioxidant enzymes, NF-kappa B p65, I kappa B alpha, TOR, Nrf2, Keap1 and apoptosis-related genes in the Fish Gill. (C) 2015 Elsevier Ltd. All rights reserved.
Lin Feng - One of the best experts on this subject based on the ideXlab platform.
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The toxic effects and potential mechanisms of deoxynivalenol on the structural integrity of Fish Gill: Oxidative damage, apoptosis and tight junctions disruption.
Toxicon, 2019Co-Authors: Chen Huang, Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Shengyao Kuang, Ling Tang, Xiaoqiu ZhouAbstract:Abstract Deoxynivalenol (DON) is a common mycotoxin existed in animal feed, and lead to significant economic loss due to its negative impacts on animal growth performance and animal health. The Gill is a primary mucosal immune organ in teleosts, and the structural integrity of the Gill is closely relevant with Fish healthy growth. Hence, this study assessed the influences of DON on the Gill structural integrity of juvenile grass carp, Ctenopharyngodan idella (initial average weight 12.17 ± 0.01 g), when offered with six different diets which contained various content of DON (27, 318, 636, 922, 1243 and 1515 μg/kg diet) for 60 days. Our research firstly systematically elaborated that DON caused histopathological lesions, oxidative injury, reduction of antioxidant ability, apoptosis as well as damages of tight junctions in Fish Gills. Comparing these data to the control, we found that DON at dose of more than 318 μg/kg diet led to oxidative injury, apoptosis and disruption of tight junctions in Fish Gill, which were likely to be relevant with Nrf2, JNK and MLCK signalling pathways, respectively. It was worth noting that DON was not found to affect the gene expressions of Keap1b (rather than Keap1a), claudin-b, claudin-3c and claudin-15b (not claudin-15a) in Fish Gills. Furthermore, based on MDA and T-AOC activities in the Gill, the maximum permissible levels of DON were evaluated to be 375.60 as well as 412.91 μg/kg diet in grass carp, respectively.
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Gill structural integrity changes in Fish deficient or excessive in dietary isoleucine towards the modulation of tight junction protein inflammation apoptosis and antioxidant defense via nf κb tor and nrf2 signaling pathways
Fish & Shellfish Immunology, 2017Co-Authors: Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Shengyao Kuang, Ling Tang, Yongan Zhang, Xiaoqiu Zhou, Wuneng TangAbstract:This study firstly aimed to test the impact of dietary isoleucine (Ile) on tight junction protein, inflammation, apoptosis, antioxidant defense and related signaling molecule gene expression in the Gill of Fish. Young grass carp (Ctenopharyngodon idella) (weighing 256.8 ± 3.5 g) were fed six diets containing graded levels of Ile, namely, 3.8, 6.6, 9.3, 12.5, 15.2 and 18.5 g/kg diet for 8 weeks. The results firstly revealed that Ile deficiency down-regulated the mRNA expressions of claudin-3, claudin-b, claudin-c, occludin and zonula occludens-1 (ZO-1) and up-regulated the mRNA expression of claudin-12, which led to the intercellular structure damage of Fish Gill. These effects were partially ascribed to the up-regulation of pro-inflammatory cytokines [interleukin 1β (IL-1β), interleukin 8 (IL-8) and tumor necrosis factor-α (TNF-α)] mRNA expressions that referring to up-regulated nuclear factor κB P65 (NF-κB P65) mRNA expression and down-regulated inhibitor factor κBα (IκBα) mRNA expression, and the down-regulation of anti-inflammatory cytokines [interleukin 10 (IL-10) and transforming growth factor β1 (TGF-β1)] mRNA expressions that referring to the down-regulated TOR and S6K1 mRNA expression. Interestingly, no change in claudin 15 mRNA level was observed among every treatment. At the same time, the results firstly indicated that Ile deficiency also resulted in the cellular structure damage of Fish Gill: (1) DNA fragmentation partially due to the up-regulation of caspase-3, caspase-8 and caspase-9 mRNA expression; (2) increase in protein carbonyl (PC), malondialdehyde (MDA) and ROS contents, which may be partially attributed to the impaired antioxidant defense [indicated by decreased glutathione (GSH) level and depressed anti-superoxide anion (ASA), anti-hydroxyl radical (a-HR), copper/zinc superoxide dismutase (Cu/Zn-SOD), catalase (CAT) and glutathione peroxidase (GPx) activities] that referring to the down-regulation of corresponding antioxidant enzyme mRNA expressions and the related signaling molecules Nrf2 mRNA expression. Ile excess caused similar negative effects that observed in Ile-deficient group, whereas these negative effects were reversed with appropriate Ile supplementation. In conclusion, our results indicated that Ile deficiency or excess disrupted the structural integrity of Fish Gill, partially due to the trigger of apoptosis, the impairment of antioxidant defense, and the regulation of tight junction protein, inflammatory cytokines, apoptosis-related, antioxidant enzymes and related signaling molecules mRNA expressions in the Fish Gill.
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thiamin deficiency induces impaired Fish Gill immune responses tight junction protein expression and antioxidant capacity roles of the nf κb tor p38 mapk and nrf2 signaling molecules
Fish & Shellfish Immunology, 2016Co-Authors: Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Juan Zhao, Shengyao KuangAbstract:In this study, we investigate the effects of dietary thiamin deficiency on immune responses, tight junctions, antioxidant capacity and related signaling molecules in the Gills of young grass carp (Ctenopharyngodon idella). Fish were fed diets that contained 0.12–2.04 mg thiamin kg−1 for 8 weeks. We found that dietary thiamin deficiency resulted in reduced complement 3 content, lysozyme and acid phosphatase activities, mRNA levels of hepcidin, liver-expressed antimicrobial peptides 2, transforming growth factor (TGF)-β1, interleukin (IL)-10, inhibitor protein-κBα (IκBα), ribosomal S6 protein kinase 1 and target of rapamycin (TOR) and increased expression of interferon-γ2, tumor necrosis factor-α, TGF-β2, IL-1β, IL-8, IκB kinases (IKKβ and IKKγ) and nuclear factor-κB p65 (NF-κB p65). Our findings showed that thiamin deficiency reduced the immune status of Fish Gills. Furthermore, thiamin deficiency resulted in reduced mRNA transcript levels of claudin b, claudin 3, claudin 12, zonula occludens 1 (ZO-1) and occludin and increased mRNA transcript levels of claudin 15a, myosin light-chain kinase (MLCK) and p38 mitogen-activated protein kinase (p38 MAPK) in Fish Gill tissues. These data suggested that thiamin deficiency disrupted tight junction-mediated Fish Gill barrier function. Additionally, reactive oxygen species, malondialdehyde and protein carbonyl levels and both the activities and expression levels of Cu/Zn superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferases and glutathione reductase, as well as NF-E2-related factor 2 gene expression in Fish Gills, were lower in Fish fed a thiamin-deficient diet. By contrast, thiamin deficiency increased levels of Kelch-like-ECH-associated protein 1a (Keap1a) and Keap1b mRNA transcript expression in Fish Gills. Taken together, our findings indicated that thiamin deficiency impaired Fish Gill health by effects on the expression of genes encoding cytokines, tight junction proteins, antioxidant enzymes, NF-κB p65, MLCK and Nrf2.
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changes in barrier health status of the Gill for grass carp ctenopharyngodon idella during valine deficiency regulation of tight junction protein transcript antioxidant status and apoptosis related gene expression
Fish & Shellfish Immunology, 2015Co-Authors: Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Shengyao Kuang, Ling Tang, Yongan Zhang, Xiaoqiu ZhouAbstract:This study investigated the effects of dietary valine on tight junction protein transcription, antioxidant status and apoptosis on grass carp Gills (Ctenopharyngodon idella). Fish were fed six different experimental diets containing graded levels of valine (4.3, 8.0, 10.6, 13.1, 16.7, 19.1 g/kg). The results indicated that valine deficiency decreased Claudin b, Claudin 3, Occludin and ZO-1 transcription and increased Claudin 15 expression in the Fish Gill (P 0.05). Valine deficiency also disrupted antioxidant status in the Gill by decreasing anti-superoxide radicals and hydroxyl radical capacity, glutathione contents and the activities and mRNA levels of Cu/Zn superoxide dismutase (SOD1), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST) (P < 0.05). These results may be ascribed to the down-regulation of NF-E2-related factor 2 (Nrf2), target of rapamycin (TOR) and ribosomal protein S6 kinase 1 (S6K1) and the up-regulation of Kelch-like-ECH-associated protein 1 (Keap1) (P < 0.05). Additionally, valine deficiency induced DNA fragmentation via the up-regulation of Caspase 3, Caspase 8 and Caspase 9 expressions (P < 0.05). These results may be ascribed to the improvement in ROS levels in the Fish Gill (P < 0.05). Taken together, the results showed that valine deficiency impaired the structural integrity of Fish Gill by disrupted Fish antioxidant defenses and regulating the expression of tight junction protein, cytokines, antioxidant enzymes, NF-kappa B p65, I kappa B alpha, TOR, Nrf2, Keap1 and apoptosis-related genes in the Fish Gill. (C) 2015 Elsevier Ltd. All rights reserved.
Nic R Bury - One of the best experts on this subject based on the ideXlab platform.
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the use of molecular descriptors to model pharmaceutical uptake by a Fish primary Gill cell culture epithelium
Environmental Science & Technology, 2019Co-Authors: Elisabeth Chang, Christer Hogstrand, Nic R Bury, Thomas H Miller, Stewart F OwenAbstract:Modeling approaches such as quantitative structure–activity relationships (QSARs) use molecular descriptors to predict the bioavailable properties of a compound in biota. However, these models have mainly been derived based on empirical data for lipophilic neutral compounds and may not predict the uptake of ionizable compounds. The majority of pharmaceuticals are ionizable, and freshwaters can have a range of pH values that affect speciation. In this study, we assessed the uptake of 10 pharmaceuticals (acetazolamide, beclomethasone, carbamazepine, diclofenac, gemfibrozil, ibuprofen, ketoprofen, norethindrone, propranolol, and warfarin) with differing modes of action and physicochemical properties (pKa, log S, log D, log Kow, molecular weight (MW), and polar surface area (PSA)) by an in vitro primary Fish Gill cell culture system (FIGCS) for 24 h in artificial freshwater. Principal component analysis (PCA) and partial least-squares (PLS) regression was used to determine the molecular descriptors that influ...
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environmental monitoring of urban streams using a primary Fish Gill cell culture system figcs
Ecotoxicology and Environmental Safety, 2015Co-Authors: Sabine Schnell, Christer Hogstrand, K A Bawaallah, Adebayo A Otitoloju, Thomas H Miller, Leon Barron, Nic R BuryAbstract:Abstract The primary Fish Gill cell culture system (FIGCS) is an in vitro technique which has the potential to replace animals in whole effluent toxicity tests. In the current study FIGCS were transported into the field and exposed to filtered (0.2 μm) river water for 24 h from 4 sites, on 2 different sampling dates. Sites 1 and 2 are situated in an urban catchment (River Wandle, London, UK) with site 1 downstream of a sewage treatment work; site 3 is located in a suburban park (River Cray, Kent, UK), and site 4 is more rural (River Darent, Kent, UK). The change in transepithelial electrical resistance (TER), the expression of the metal responsive genes metallothionein A ( mta ) and B ( mtb ), cytochrome P450 1A1 ( cyp1a1 ) and 3A27 ( cyp3a27 ), involved in phase 1 metabolism, were assessed following exposure to sample water for 24 h. TER was comparable between FIGCS exposed to 0.2 μm filtered river water and those exposed to synthetic moderately soft water for 24 h. During the first sampling time, there was an increase in mta , cyp1a1 and cyp3a27 gene expression in epithelium exposed to water from sites 1 and 2, and during the second sampling period an increase in cyp3a27 gene expression at sites 1 and 4. Urban river water is a complex mixture of contaminants (e.g., metals, pesticides, pharmaceuticals and polyaromatic hydrocarbons) and the increase in the expression of genes encoding mta , cyp1a1 and cyp3a27 in FIGCS is indicative of the presence of biologically active pollutants.
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a primary Fish Gill cell culture model to assess pharmaceutical uptake and efflux evidence for passive and facilitated transport
Aquatic Toxicology, 2015Co-Authors: Sabine Schnell, Christer Hogstrand, Stewart F Owen, Lucy C Stott, Nic R BuryAbstract:The Gill is the principle site of xenobiotic transfer to and from the aqueous environment. To replace, refine or reduce (3Rs) the large numbers of Fish used in in vivo uptake studies an effective in vitro screen is required that mimics the function of the teleost Gill. This study uses a rainbow trout (Oncorhynchus mykiss) primary Gill cell culture system grown on permeable inserts, which tolerates apical freshwater thus mimicking the intact organ, to assess the uptake and efflux of pharmaceuticals across the Gill. Bidirectional transport studies in media of seven pharmaceuticals (propranolol, metoprolol, atenolol, formoterol, terbutaline, ranitidine and imipramine) showed they were transported transcellularly across the epithelium. However, studies conducted in water showed enhanced uptake of propranolol, ranitidine and imipramine. Concentration-equilibrated conditions without a concentration gradient suggested that a proportion of the uptake of propranolol and imipramine is via a carrier-mediated process. Further study using propranolol showed that its transport is pH-dependent and at very low environmentally relevant concentrations (ng L−1), transport deviated from linearity. At higher concentrations, passive uptake dominated. Known inhibitors of drug transport proteins; cimetidine, MK571, cyclosporine A and quinidine inhibited propranolol uptake, whilst amantadine and verapamil were without effect. Together this suggests the involvement of specific members of SLC and ABC drug transporter families in pharmaceutical transport.
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a primary Fish Gill cell system figcs for environmental monitoring of river waters
Aquatic Toxicology, 2014Co-Authors: Matteo Minghetti, Sabine Schnell, Michael A Chadwick, Christer Hogstrand, Nic R BuryAbstract:Studies were conducted to assess the feasibility of a primary Fish Gill Cell culture system (FIGCS) for both laboratory and field based environmental monitoring of rivers known to be affected by metal contamination. FIGCS were exposed in the laboratory and in the field to water from the River Hayle, a metal-contaminated system in Cornwall, United Kingdom. Water chemistry, including transition metal concentrations, changes in transepithelial electrical resistance (TEER), cell viability and the expression of metal responsive genes, metallothionein A and B were measured. FIGCS tolerated river water in the laboratory showing no loss in TEER or cell viability following 24 h exposure. The cells also tolerated transport to the field (∼1000 km and 30 h) and exposure to unfiltered and filtered river water. Metallothionein A and B, a measure of intracellular biologically active metals, expression was induced in the laboratory and field on exposure to water from sites with elevated metal concentrations compared to those sites where metal levels were below water metal Environmental Quality Standards. This demonstrates that FIGCS detects bioreactive metals in river waters on exposure in the laboratory or field and can be used for on-site environmental monitoring as well as investigations into bioavailability and toxicity of contaminant mixtures in natural waters.
Shengyao Kuang - One of the best experts on this subject based on the ideXlab platform.
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The toxic effects and potential mechanisms of deoxynivalenol on the structural integrity of Fish Gill: Oxidative damage, apoptosis and tight junctions disruption.
Toxicon, 2019Co-Authors: Chen Huang, Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Shengyao Kuang, Ling Tang, Xiaoqiu ZhouAbstract:Abstract Deoxynivalenol (DON) is a common mycotoxin existed in animal feed, and lead to significant economic loss due to its negative impacts on animal growth performance and animal health. The Gill is a primary mucosal immune organ in teleosts, and the structural integrity of the Gill is closely relevant with Fish healthy growth. Hence, this study assessed the influences of DON on the Gill structural integrity of juvenile grass carp, Ctenopharyngodan idella (initial average weight 12.17 ± 0.01 g), when offered with six different diets which contained various content of DON (27, 318, 636, 922, 1243 and 1515 μg/kg diet) for 60 days. Our research firstly systematically elaborated that DON caused histopathological lesions, oxidative injury, reduction of antioxidant ability, apoptosis as well as damages of tight junctions in Fish Gills. Comparing these data to the control, we found that DON at dose of more than 318 μg/kg diet led to oxidative injury, apoptosis and disruption of tight junctions in Fish Gill, which were likely to be relevant with Nrf2, JNK and MLCK signalling pathways, respectively. It was worth noting that DON was not found to affect the gene expressions of Keap1b (rather than Keap1a), claudin-b, claudin-3c and claudin-15b (not claudin-15a) in Fish Gills. Furthermore, based on MDA and T-AOC activities in the Gill, the maximum permissible levels of DON were evaluated to be 375.60 as well as 412.91 μg/kg diet in grass carp, respectively.
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Gill structural integrity changes in Fish deficient or excessive in dietary isoleucine towards the modulation of tight junction protein inflammation apoptosis and antioxidant defense via nf κb tor and nrf2 signaling pathways
Fish & Shellfish Immunology, 2017Co-Authors: Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Shengyao Kuang, Ling Tang, Yongan Zhang, Xiaoqiu Zhou, Wuneng TangAbstract:This study firstly aimed to test the impact of dietary isoleucine (Ile) on tight junction protein, inflammation, apoptosis, antioxidant defense and related signaling molecule gene expression in the Gill of Fish. Young grass carp (Ctenopharyngodon idella) (weighing 256.8 ± 3.5 g) were fed six diets containing graded levels of Ile, namely, 3.8, 6.6, 9.3, 12.5, 15.2 and 18.5 g/kg diet for 8 weeks. The results firstly revealed that Ile deficiency down-regulated the mRNA expressions of claudin-3, claudin-b, claudin-c, occludin and zonula occludens-1 (ZO-1) and up-regulated the mRNA expression of claudin-12, which led to the intercellular structure damage of Fish Gill. These effects were partially ascribed to the up-regulation of pro-inflammatory cytokines [interleukin 1β (IL-1β), interleukin 8 (IL-8) and tumor necrosis factor-α (TNF-α)] mRNA expressions that referring to up-regulated nuclear factor κB P65 (NF-κB P65) mRNA expression and down-regulated inhibitor factor κBα (IκBα) mRNA expression, and the down-regulation of anti-inflammatory cytokines [interleukin 10 (IL-10) and transforming growth factor β1 (TGF-β1)] mRNA expressions that referring to the down-regulated TOR and S6K1 mRNA expression. Interestingly, no change in claudin 15 mRNA level was observed among every treatment. At the same time, the results firstly indicated that Ile deficiency also resulted in the cellular structure damage of Fish Gill: (1) DNA fragmentation partially due to the up-regulation of caspase-3, caspase-8 and caspase-9 mRNA expression; (2) increase in protein carbonyl (PC), malondialdehyde (MDA) and ROS contents, which may be partially attributed to the impaired antioxidant defense [indicated by decreased glutathione (GSH) level and depressed anti-superoxide anion (ASA), anti-hydroxyl radical (a-HR), copper/zinc superoxide dismutase (Cu/Zn-SOD), catalase (CAT) and glutathione peroxidase (GPx) activities] that referring to the down-regulation of corresponding antioxidant enzyme mRNA expressions and the related signaling molecules Nrf2 mRNA expression. Ile excess caused similar negative effects that observed in Ile-deficient group, whereas these negative effects were reversed with appropriate Ile supplementation. In conclusion, our results indicated that Ile deficiency or excess disrupted the structural integrity of Fish Gill, partially due to the trigger of apoptosis, the impairment of antioxidant defense, and the regulation of tight junction protein, inflammatory cytokines, apoptosis-related, antioxidant enzymes and related signaling molecules mRNA expressions in the Fish Gill.
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thiamin deficiency induces impaired Fish Gill immune responses tight junction protein expression and antioxidant capacity roles of the nf κb tor p38 mapk and nrf2 signaling molecules
Fish & Shellfish Immunology, 2016Co-Authors: Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Juan Zhao, Shengyao KuangAbstract:In this study, we investigate the effects of dietary thiamin deficiency on immune responses, tight junctions, antioxidant capacity and related signaling molecules in the Gills of young grass carp (Ctenopharyngodon idella). Fish were fed diets that contained 0.12–2.04 mg thiamin kg−1 for 8 weeks. We found that dietary thiamin deficiency resulted in reduced complement 3 content, lysozyme and acid phosphatase activities, mRNA levels of hepcidin, liver-expressed antimicrobial peptides 2, transforming growth factor (TGF)-β1, interleukin (IL)-10, inhibitor protein-κBα (IκBα), ribosomal S6 protein kinase 1 and target of rapamycin (TOR) and increased expression of interferon-γ2, tumor necrosis factor-α, TGF-β2, IL-1β, IL-8, IκB kinases (IKKβ and IKKγ) and nuclear factor-κB p65 (NF-κB p65). Our findings showed that thiamin deficiency reduced the immune status of Fish Gills. Furthermore, thiamin deficiency resulted in reduced mRNA transcript levels of claudin b, claudin 3, claudin 12, zonula occludens 1 (ZO-1) and occludin and increased mRNA transcript levels of claudin 15a, myosin light-chain kinase (MLCK) and p38 mitogen-activated protein kinase (p38 MAPK) in Fish Gill tissues. These data suggested that thiamin deficiency disrupted tight junction-mediated Fish Gill barrier function. Additionally, reactive oxygen species, malondialdehyde and protein carbonyl levels and both the activities and expression levels of Cu/Zn superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferases and glutathione reductase, as well as NF-E2-related factor 2 gene expression in Fish Gills, were lower in Fish fed a thiamin-deficient diet. By contrast, thiamin deficiency increased levels of Kelch-like-ECH-associated protein 1a (Keap1a) and Keap1b mRNA transcript expression in Fish Gills. Taken together, our findings indicated that thiamin deficiency impaired Fish Gill health by effects on the expression of genes encoding cytokines, tight junction proteins, antioxidant enzymes, NF-κB p65, MLCK and Nrf2.
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changes in barrier health status of the Gill for grass carp ctenopharyngodon idella during valine deficiency regulation of tight junction protein transcript antioxidant status and apoptosis related gene expression
Fish & Shellfish Immunology, 2015Co-Authors: Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Shengyao Kuang, Ling Tang, Yongan Zhang, Xiaoqiu ZhouAbstract:This study investigated the effects of dietary valine on tight junction protein transcription, antioxidant status and apoptosis on grass carp Gills (Ctenopharyngodon idella). Fish were fed six different experimental diets containing graded levels of valine (4.3, 8.0, 10.6, 13.1, 16.7, 19.1 g/kg). The results indicated that valine deficiency decreased Claudin b, Claudin 3, Occludin and ZO-1 transcription and increased Claudin 15 expression in the Fish Gill (P 0.05). Valine deficiency also disrupted antioxidant status in the Gill by decreasing anti-superoxide radicals and hydroxyl radical capacity, glutathione contents and the activities and mRNA levels of Cu/Zn superoxide dismutase (SOD1), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST) (P < 0.05). These results may be ascribed to the down-regulation of NF-E2-related factor 2 (Nrf2), target of rapamycin (TOR) and ribosomal protein S6 kinase 1 (S6K1) and the up-regulation of Kelch-like-ECH-associated protein 1 (Keap1) (P < 0.05). Additionally, valine deficiency induced DNA fragmentation via the up-regulation of Caspase 3, Caspase 8 and Caspase 9 expressions (P < 0.05). These results may be ascribed to the improvement in ROS levels in the Fish Gill (P < 0.05). Taken together, the results showed that valine deficiency impaired the structural integrity of Fish Gill by disrupted Fish antioxidant defenses and regulating the expression of tight junction protein, cytokines, antioxidant enzymes, NF-kappa B p65, I kappa B alpha, TOR, Nrf2, Keap1 and apoptosis-related genes in the Fish Gill. (C) 2015 Elsevier Ltd. All rights reserved.
Weidan Jiang - One of the best experts on this subject based on the ideXlab platform.
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The toxic effects and potential mechanisms of deoxynivalenol on the structural integrity of Fish Gill: Oxidative damage, apoptosis and tight junctions disruption.
Toxicon, 2019Co-Authors: Chen Huang, Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Shengyao Kuang, Ling Tang, Xiaoqiu ZhouAbstract:Abstract Deoxynivalenol (DON) is a common mycotoxin existed in animal feed, and lead to significant economic loss due to its negative impacts on animal growth performance and animal health. The Gill is a primary mucosal immune organ in teleosts, and the structural integrity of the Gill is closely relevant with Fish healthy growth. Hence, this study assessed the influences of DON on the Gill structural integrity of juvenile grass carp, Ctenopharyngodan idella (initial average weight 12.17 ± 0.01 g), when offered with six different diets which contained various content of DON (27, 318, 636, 922, 1243 and 1515 μg/kg diet) for 60 days. Our research firstly systematically elaborated that DON caused histopathological lesions, oxidative injury, reduction of antioxidant ability, apoptosis as well as damages of tight junctions in Fish Gills. Comparing these data to the control, we found that DON at dose of more than 318 μg/kg diet led to oxidative injury, apoptosis and disruption of tight junctions in Fish Gill, which were likely to be relevant with Nrf2, JNK and MLCK signalling pathways, respectively. It was worth noting that DON was not found to affect the gene expressions of Keap1b (rather than Keap1a), claudin-b, claudin-3c and claudin-15b (not claudin-15a) in Fish Gills. Furthermore, based on MDA and T-AOC activities in the Gill, the maximum permissible levels of DON were evaluated to be 375.60 as well as 412.91 μg/kg diet in grass carp, respectively.
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Gill structural integrity changes in Fish deficient or excessive in dietary isoleucine towards the modulation of tight junction protein inflammation apoptosis and antioxidant defense via nf κb tor and nrf2 signaling pathways
Fish & Shellfish Immunology, 2017Co-Authors: Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Shengyao Kuang, Ling Tang, Yongan Zhang, Xiaoqiu Zhou, Wuneng TangAbstract:This study firstly aimed to test the impact of dietary isoleucine (Ile) on tight junction protein, inflammation, apoptosis, antioxidant defense and related signaling molecule gene expression in the Gill of Fish. Young grass carp (Ctenopharyngodon idella) (weighing 256.8 ± 3.5 g) were fed six diets containing graded levels of Ile, namely, 3.8, 6.6, 9.3, 12.5, 15.2 and 18.5 g/kg diet for 8 weeks. The results firstly revealed that Ile deficiency down-regulated the mRNA expressions of claudin-3, claudin-b, claudin-c, occludin and zonula occludens-1 (ZO-1) and up-regulated the mRNA expression of claudin-12, which led to the intercellular structure damage of Fish Gill. These effects were partially ascribed to the up-regulation of pro-inflammatory cytokines [interleukin 1β (IL-1β), interleukin 8 (IL-8) and tumor necrosis factor-α (TNF-α)] mRNA expressions that referring to up-regulated nuclear factor κB P65 (NF-κB P65) mRNA expression and down-regulated inhibitor factor κBα (IκBα) mRNA expression, and the down-regulation of anti-inflammatory cytokines [interleukin 10 (IL-10) and transforming growth factor β1 (TGF-β1)] mRNA expressions that referring to the down-regulated TOR and S6K1 mRNA expression. Interestingly, no change in claudin 15 mRNA level was observed among every treatment. At the same time, the results firstly indicated that Ile deficiency also resulted in the cellular structure damage of Fish Gill: (1) DNA fragmentation partially due to the up-regulation of caspase-3, caspase-8 and caspase-9 mRNA expression; (2) increase in protein carbonyl (PC), malondialdehyde (MDA) and ROS contents, which may be partially attributed to the impaired antioxidant defense [indicated by decreased glutathione (GSH) level and depressed anti-superoxide anion (ASA), anti-hydroxyl radical (a-HR), copper/zinc superoxide dismutase (Cu/Zn-SOD), catalase (CAT) and glutathione peroxidase (GPx) activities] that referring to the down-regulation of corresponding antioxidant enzyme mRNA expressions and the related signaling molecules Nrf2 mRNA expression. Ile excess caused similar negative effects that observed in Ile-deficient group, whereas these negative effects were reversed with appropriate Ile supplementation. In conclusion, our results indicated that Ile deficiency or excess disrupted the structural integrity of Fish Gill, partially due to the trigger of apoptosis, the impairment of antioxidant defense, and the regulation of tight junction protein, inflammatory cytokines, apoptosis-related, antioxidant enzymes and related signaling molecules mRNA expressions in the Fish Gill.
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thiamin deficiency induces impaired Fish Gill immune responses tight junction protein expression and antioxidant capacity roles of the nf κb tor p38 mapk and nrf2 signaling molecules
Fish & Shellfish Immunology, 2016Co-Authors: Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Juan Zhao, Shengyao KuangAbstract:In this study, we investigate the effects of dietary thiamin deficiency on immune responses, tight junctions, antioxidant capacity and related signaling molecules in the Gills of young grass carp (Ctenopharyngodon idella). Fish were fed diets that contained 0.12–2.04 mg thiamin kg−1 for 8 weeks. We found that dietary thiamin deficiency resulted in reduced complement 3 content, lysozyme and acid phosphatase activities, mRNA levels of hepcidin, liver-expressed antimicrobial peptides 2, transforming growth factor (TGF)-β1, interleukin (IL)-10, inhibitor protein-κBα (IκBα), ribosomal S6 protein kinase 1 and target of rapamycin (TOR) and increased expression of interferon-γ2, tumor necrosis factor-α, TGF-β2, IL-1β, IL-8, IκB kinases (IKKβ and IKKγ) and nuclear factor-κB p65 (NF-κB p65). Our findings showed that thiamin deficiency reduced the immune status of Fish Gills. Furthermore, thiamin deficiency resulted in reduced mRNA transcript levels of claudin b, claudin 3, claudin 12, zonula occludens 1 (ZO-1) and occludin and increased mRNA transcript levels of claudin 15a, myosin light-chain kinase (MLCK) and p38 mitogen-activated protein kinase (p38 MAPK) in Fish Gill tissues. These data suggested that thiamin deficiency disrupted tight junction-mediated Fish Gill barrier function. Additionally, reactive oxygen species, malondialdehyde and protein carbonyl levels and both the activities and expression levels of Cu/Zn superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferases and glutathione reductase, as well as NF-E2-related factor 2 gene expression in Fish Gills, were lower in Fish fed a thiamin-deficient diet. By contrast, thiamin deficiency increased levels of Kelch-like-ECH-associated protein 1a (Keap1a) and Keap1b mRNA transcript expression in Fish Gills. Taken together, our findings indicated that thiamin deficiency impaired Fish Gill health by effects on the expression of genes encoding cytokines, tight junction proteins, antioxidant enzymes, NF-κB p65, MLCK and Nrf2.
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changes in barrier health status of the Gill for grass carp ctenopharyngodon idella during valine deficiency regulation of tight junction protein transcript antioxidant status and apoptosis related gene expression
Fish & Shellfish Immunology, 2015Co-Authors: Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Shengyao Kuang, Ling Tang, Yongan Zhang, Xiaoqiu ZhouAbstract:This study investigated the effects of dietary valine on tight junction protein transcription, antioxidant status and apoptosis on grass carp Gills (Ctenopharyngodon idella). Fish were fed six different experimental diets containing graded levels of valine (4.3, 8.0, 10.6, 13.1, 16.7, 19.1 g/kg). The results indicated that valine deficiency decreased Claudin b, Claudin 3, Occludin and ZO-1 transcription and increased Claudin 15 expression in the Fish Gill (P 0.05). Valine deficiency also disrupted antioxidant status in the Gill by decreasing anti-superoxide radicals and hydroxyl radical capacity, glutathione contents and the activities and mRNA levels of Cu/Zn superoxide dismutase (SOD1), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST) (P < 0.05). These results may be ascribed to the down-regulation of NF-E2-related factor 2 (Nrf2), target of rapamycin (TOR) and ribosomal protein S6 kinase 1 (S6K1) and the up-regulation of Kelch-like-ECH-associated protein 1 (Keap1) (P < 0.05). Additionally, valine deficiency induced DNA fragmentation via the up-regulation of Caspase 3, Caspase 8 and Caspase 9 expressions (P < 0.05). These results may be ascribed to the improvement in ROS levels in the Fish Gill (P < 0.05). Taken together, the results showed that valine deficiency impaired the structural integrity of Fish Gill by disrupted Fish antioxidant defenses and regulating the expression of tight junction protein, cytokines, antioxidant enzymes, NF-kappa B p65, I kappa B alpha, TOR, Nrf2, Keap1 and apoptosis-related genes in the Fish Gill. (C) 2015 Elsevier Ltd. All rights reserved.