Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 8 de 8
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Aquat Toxicol ; 239: 105956, 2021 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-34496328

RESUMO

Intensive aquaculture often results in immunosuppression in fish, which may cause a series of diseases. In this study, to investigate the immunosuppressive mechanisms in fish, tilapia were intrapleural injected cyclophosphamide (CTX) at the doses of 10, 25, 50, 75 and 100 mg·kg-1 to induce immunosuppression. We determined the viability of immune cells, the content of lysozyme (LZM) and immunoglobulin M (IgM), the levels of nitric oxide (NO) and antioxidant parameters. Meanwhile, the mRNA levels of complement C3 (c3), igm and the genes associated with the TLR-NF-κB signaling pathway in the head kidney (HK) and spleen were also determined. The results showed that CTX had a significant cytotoxic effect on peripheral blood leukocytes, HK macrophages and spleen cells in a dose-dependent manner. The protein and mRNA levels of C3 and IgM were down-regulated with the increase of CTX concentrations in serum, HK and/or spleen. The NO and LZM contents decreased significantly in HK and spleen after CTX treatments with 75 and 100 mg·kg-1. CTX treatments with 50, 75 and/or 100 mg·kg-1 markedly decreased the antioxidant ability and enhanced lipid peroxidation in HK and spleen. Furthermore, qPCR data showed that CTX treatments with 50-100 mg·kg-1 clearly down-regulated the mRNA levels of tlr2, myd88, irak1, traf6, nfκb1, nfκb2, il-6, il-10 and tnf-α in the HK and/or spleen. Overall results suggested that CTX treatment had a cytotoxic effect on immune cells, induced lipid peroxidation, decreased the antioxidant capacity and inhibited immune function. The immunosuppressive mechanisms of CTX may be associated with the TLR-NF-κB signaling pathway.


Assuntos
Ciclídeos , Doenças dos Peixes , Poluentes Químicos da Água , Animais , Antioxidantes , Ciclídeos/metabolismo , Ciclofosfamida/toxicidade , Imunidade , NF-kappa B/genética , NF-kappa B/metabolismo , Transdução de Sinais , Poluentes Químicos da Água/toxicidade
2.
Res Vet Sci ; 138: 167-177, 2021 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-34153557

RESUMO

Adhesion molecules play an important role in urinary calculus formation. The expressions of adhesion molecules in renal tubular has been reported in some animals. However, the role of adhesion molecules in the process of sheep urinary calculus formation is still unclear. The magnesium ammonium phosphate (MAP) is the main component of sheep urinary calculus. In this paper, the sheep renal tubular epithelial cells (RTECs) were isolated and treated with MAP, the expressions of osteopontin (OPN), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and apoptosis-related indicators caspase-3, Bcl-2 and Bax in RTECs were observed, the viability of RTECs was detected by Cell Counting Kit-8 (CCK-8). The levels of superoxide dismutase (SOD) and malondialdehyde (MDA), and the expressions of inflammatory factors Interleukin-6 (IL-6), Interleukin-1 (IL-1), Interleukin-17 (IL-17) and tumor necrosis factor-α (TNF-α) were measured by enzyme-linked immunosorbent (ELISA). The histopathological observation of kidney in urolithiasis sheep was made. The results showed that MAP could reduce the viability and SOD activity, enhance the activity of MDA significantly and promote the expressions of IL-1, IL-6, IL-17 and TNF-α of RTECs. By western blot and qPCR methods, the expressions of ICAM-1, VCAM-1 and OPN increased in 48 h. In addition, the expression of caspase-3 increased significantly and the ratio of Bcl-2/Bax reduced with exposure to MAP. The renal tissue structure was seriously damaged, the RTECs in urolithiasis sheep were degenerative and necrotic.


Assuntos
Apoptose , Moléculas de Adesão Celular/metabolismo , Sobrevivência Celular , Citocinas/imunologia , Células Epiteliais/fisiologia , Estresse Oxidativo , Estruvita/metabolismo , Animais , Células Cultivadas , Molécula 1 de Adesão Intercelular/metabolismo , Rim/fisiologia , Osteopontina/metabolismo , Carneiro Doméstico/metabolismo , Carneiro Doméstico/urina , Cálculos Urinários/metabolismo , Molécula 1 de Adesão de Célula Vascular/metabolismo
3.
Fish Shellfish Immunol ; 104: 391-401, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32553566

RESUMO

Fatty liver injury (or disease) is a common disease in farmed fish, but its pathogenic mechanism is not fully understood. Therefore the present study aims to investigate high-fat diet (HFD)-induced liver injury and explore the underlying mechanism in fish. The tilapia were fed on control diet and HFD for 90 days, and then the blood and liver tissues were collected to determine biochemical parameter, gene expression and protein level. The results showed that HFD feeding signally increased the levels of plasma aminotransferases and pro-inflammatory factors after 60 days. In liver and plasma, HFD feeding significantly suppressed antioxidant ability, but enhanced lipid peroxidation formation, protein oxidation and DNA damage after 60 or 90 days. Further, the Nrf2 pathway and antioxidative function-related genes were adversely changed in liver of HFD-fed tilapia after 60 and/or 90 days. Meanwhile, HFD treatment induced apoptosis via initiating mitochondrial pathway in liver after 90 days. Furthermore, after 90 days of feeding, the expression of genes or proteins related to JNK pathway and TLRs-Myd88-NF-κB pathway was clearly upregulated in HFD treatment. Similarly, the mRNA levels of inflammatory factors including tumor necrosis factor (TNF-α), interleukin-1ß (IL-1ß), IL-6, IL-8 and IL-10 were also upregulated in liver of HFD-fed tilapia after 60 and/or 90 days. In conclusion, the current study suggested that HFD feeding impaired antioxidant defense system, induced apoptosis, enhanced inflammation and led to liver injury. The adverse influences of HFD in the liver might be due to the variation of Nrf2, JNK and TLRs-Myd88-NF-κB signaling pathways.


Assuntos
Antioxidantes/metabolismo , Apoptose/efeitos dos fármacos , Ciclídeos/fisiologia , Dieta Hiperlipídica/veterinária , Inflamação/veterinária , Transdução de Sinais/imunologia , Animais , Ciclídeos/imunologia , Ciclídeos/metabolismo , Dieta Hiperlipídica/efeitos adversos , Doenças dos Peixes/fisiopatologia , Proteínas de Peixes/imunologia , Inflamação/fisiopatologia , Hepatopatias/fisiopatologia , Hepatopatias/veterinária , Sistema de Sinalização das MAP Quinases/imunologia , Fator 2 Relacionado a NF-E2/imunologia , Receptores Toll-Like/imunologia
4.
In Vitro Cell Dev Biol Anim ; 52(1): 1-9, 2016 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-26481798

RESUMO

The present study was to investigate the protective effect and possible mechanism of phyllanthin against carbon tetrachloride (CCl4)-induced hepatocyte damage in carp. Phyllanthin (5, 10, and 15 µg/ml) was added to carp primary hepatocytes before (pre-treatment) and after (post-treatment) incubation of the hepatocytes in medium containing CCl4 at 8 mM; supernatant and cell were collected for the analyses of cell viability, biochemical parameters, and gene expression. The results showed that phyllanthin at the concentration of 15 µg/ml significantly suppressed the elevation of glutamate pyruvate transaminase (GPT), glutamate oxalate transaminase (GOT), lactate dehydrogenase (LDH), and malondialdehyde (MDA), and the reduction of cell viability, superoxide dismutase (SOD) activity, cytochrome P450 1a (CYP1A), and cytochrome P450 3a (CYP3A) messenger RNA (mRNA) levels expect LDH in the post-treatment. The levels of GPT, GOT, and CYP1A mRNA were also effectively restored in the pretreatment with phyllanthin (10 µg/ml). Overall, our results suggested that phyllanthin may be used as a hepatoprotective agent to prevent liver diseases in fish.


Assuntos
Doenças dos Peixes/tratamento farmacológico , Hepatócitos/efeitos dos fármacos , Lignanas/farmacologia , Substâncias Protetoras/farmacologia , Animais , Tetracloreto de Carbono/toxicidade , Carpas/lesões , Carpas/metabolismo , Sobrevivência Celular/efeitos dos fármacos , Doenças dos Peixes/metabolismo , Hepatócitos/metabolismo , Fígado/efeitos dos fármacos , Fígado/enzimologia , Fígado/patologia
5.
Bull Environ Contam Toxicol ; 96(1): 55-61, 2016 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-26508429

RESUMO

The aim of this study was to establish a model for the study of liver injury induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in Jian carp using precision-cut liver slices (PCLS). PCLS were treated with TCDD at concentrations of 0, 0.05, 0.1, 0.3, and 0.6 µg/L for 6 h, followed by collection of the culture supernatant and PCLS for analysis. Several biochemical indices were analyzed, including glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT), lactate dehydrogenase (LDH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA). Expression of mRNA was also estimated for cytochrome P4501A (CYP1A), aryl hydrocarbon receptor2 (AhR2), and aryl hydrocarbon receptor nuclear translocator2 (ARNT2). Results showed that some significant effects (p < 0.05) in MDA, GSH-Px and PCLS viability were observed at a TCDD concentration as low as 0.05 µg/L, and the observed effects increased with exposure concentration. Following exposure to TCDD for 6 h at a concentration of 0.3 µg/L, significant increases (p < 0.01) in the content of GPT, GOT, MDA, and LDH were observed, while SOD activity, GSH-Px activity, and PCLS viability were decreased (p < 0.01 or p < 0.05). Exposure to 0.3 µg/L TCDD also resulted in increased expression of mRNA for CYP1A, AhR2, and ARNT2. Overall, these results provide evidence of TCDD-induced liver injury and oxidative stress in Jian carp. These results also support the use of PCLS as an in vitro model for the evaluation of hepatotoxicity in Jian carp.


Assuntos
Carpas/metabolismo , Técnicas In Vitro/métodos , Fígado/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Dibenzodioxinas Policloradas/toxicidade , Animais , Glutationa Peroxidase/metabolismo , Fígado/metabolismo , Malondialdeído/metabolismo , Oxirredução , RNA Mensageiro/metabolismo , Receptores de Hidrocarboneto Arílico/metabolismo , Superóxido Dismutase/metabolismo
6.
Int Immunopharmacol ; 25(1): 112-20, 2015 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-25639226

RESUMO

The aim of this study was to investigate the anti-inflammatory and hepatoprotective effects of Ganoderma lucidum polysaccharides (GLPS) on carbon tetrachloride (CCl4)-induced hepatocyte damage in common carp (Cyprinus carpio L.). GLPS (0.1, 0.3, 0.6mg/ml) were added to the primary hepatocytes before (pre-treatment), after (post-treatment) and both before and after (pre- and post-treatment) the incubation of the hepatocytes with CCl4 at the concentration of 8mM in the culture medium. The supernatants and cells were collected respectively to detect the biochemical indicators. The levels of TNF-α, IL-1ß, caspase-3 and caspase-8 were measured by ELISA, the mRNA expressions of CYP1A and CYP3A were determined by RT-PCR, and western blotting was used to assay the relative protein expressions of c-Rel and p65. Results showed that GLPS significantly improved cell viability and inhibited the elevations of the marker enzymes (GOT, GPT, LDH) and MDA induced by CCl4, and markedly increased the level of SOD. Treatments with GLPS resulted in a significant decrease in the expressions of CYP1A and CYP3A, and significantly down-regulated extrinsic apoptosis and immune inflammatory response. In brief, the present study showed that GLPS can protect hepatocyte injury induced by CCl4 through inhibiting lipid peroxidation, elevating antioxidant enzyme activity and suppressing apoptosis and immune inflammatory response.


Assuntos
Anti-Inflamatórios/farmacologia , Polissacarídeos Fúngicos/farmacologia , Hepatócitos/efeitos dos fármacos , Medicina Tradicional Chinesa , Reishi/imunologia , Animais , Apoptose/efeitos dos fármacos , Tetracloreto de Carbono/toxicidade , Carpas , Caspase 3/metabolismo , Caspase 8/metabolismo , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Citocromo P-450 CYP1A1/genética , Citocromo P-450 CYP1A1/metabolismo , Citocromo P-450 CYP3A/genética , Citocromo P-450 CYP3A/metabolismo , Hepatócitos/patologia , Hepatócitos/fisiologia , Interleucina-1beta/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Fator de Necrose Tumoral alfa/metabolismo
7.
Virus Res ; 185: 77-81, 2014 Jun 24.
Artigo em Inglês | MEDLINE | ID: mdl-24680657

RESUMO

Grass carp hemorrhage is an acute contagious disease caused by grass carp reovirus (GCRV). The pathogenesis of GCRV and the relationship between GCRV and the host cells remain unclear. The aim of the present study was to investigate the relations among apoptosis, intracellular oxidative stress and virus replication in GCRV infected-cells. The results showed that GCRV induced activation of caspase proteases as early as 12 h, and reached maximum activities at 24 h or 48 h post-infection in a grass carp kidney cell line (CIK cells). Meanwhile, the levels of tumor necrosis factor (TNF-α) and interleukin-1ß (IL-1ß) also were increased in GCRV-infected CIK cells and showed a statistically significant difference from 24 h to 96 h post-infection. The infection of GCRV caused the destruction of entire monolayer and the death of host cells. Accompanied by the infection, a severe oxidative stress occurred, which led to extensive loss of antioxidants and formation of lipid peroxidation after 48 h post-infection. These data suggested that the apoptosis which was triggered at an early stage (12-24 h) in the viral infection cycle, might be independent of virus replication, while the oxidative stress induced by GCRV was mostly related to the virus replication.


Assuntos
Apoptose , Doenças dos Peixes/metabolismo , Infecções por Reoviridae/veterinária , Reoviridae/fisiologia , Animais , Carpas , Linhagem Celular , Doenças dos Peixes/genética , Doenças dos Peixes/fisiopatologia , Doenças dos Peixes/virologia , Proteínas de Peixes/genética , Proteínas de Peixes/metabolismo , Estresse Oxidativo , Infecções por Reoviridae/metabolismo , Infecções por Reoviridae/fisiopatologia , Infecções por Reoviridae/virologia , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismo , Replicação Viral
8.
Aquat Toxicol ; 152: 11-9, 2014 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-24721155

RESUMO

In the present study, the cellular and molecular mechanism of carbon tetrachloride (CCl4)-induced hepatotoxicity in fish was investigated by studying the effects of CCl4 on the oxidative stress, inflammatory response and hepatocyte apoptosis. Common carp were given an intraperitoneal injection of 30% CCl4 in arachis oil (0.5ml/kg body weight). At 72h post-injection, blood were collected to measure glutamate pyruvate transaminase (GPT), glutamate oxalate transaminase (GOT), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione (GSH), total antioxidant capacity (T-AOC) and malondialdehyde (MDA), liver samples were taken to analyze toll-like receptor 4 (TLR4), cytochrome P450 2E1 (CYP2E1) and gene expressions of inflammatory cytokines and nuclear factor-κB (NF-κB/cREL). Cell viability and apoptosis were analyzed after treatment of the primary hepatocytes with CCl4 at 8mM. The results showed that CCl4 significantly increased the levels of GPT, GOT, MDA, TLR4 and CYP2E1, reduced the levels of SOD, GPx, CAT, GSH and T-AOC, and up-regulated the gene expressions of NF-κB/cREL and inflammatory cytokines including tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), IL-1ß, IL-6 and IL-12. In vitro, CCl4 caused a dramatic loss in cell viability and induced hepatocyte apoptosis. Overall results suggest that oxidative stress lipid peroxidation, and TNF-α/NF-κB and TRL4/NF-κB signaling pathways play important roles in CCl4-induced hepatotoxicity in fish.


Assuntos
Apoptose/efeitos dos fármacos , Tetracloreto de Carbono/toxicidade , Carpas , Hepatócitos/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Transdução de Sinais/efeitos dos fármacos , Poluentes Químicos da Água/toxicidade , Animais , Sobrevivência Celular/efeitos dos fármacos , Citocinas/genética , Citocinas/metabolismo , Regulação da Expressão Gênica/efeitos dos fármacos , Peroxidação de Lipídeos/efeitos dos fármacos , NF-kappa B/genética , NF-kappa B/metabolismo , Necrose/induzido quimicamente , Oxirredutases/genética , Oxirredutases/metabolismo
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...