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NIBV is an acute and highly contagious virus that has a major impact on the poultry industry. Wogonin, as a flavonoid drug, has antiviral effects, but there have been no reports indicating its role in renal injury caused by NIBV infection. The aim of this study is to investigate the antiviral effect of wogonin against NIBV. Renal tubular epithelial cells were isolated and cultured, and divided into four groups: Con, Con+Wog, NIBV and NIBV+Wog. We found that wogonin significantly inhibited the copy number of NIBV and significantly alleviated NIBV-induced cell apoptosis and necrosis. Moreover, wogonin inhibited the reduction in mitochondrial membrane potential and the aberrant opening of mPTP caused by NIBV. In conclusion, wogonin can protect renal tubular epithelial cells from damage by inhibiting the replication of NIBV and preventing mitochondrial apoptosis and necroptosis induced by NIBV.
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Apoptosis , Pollos , Células Epiteliales , Flavanonas , Túbulos Renales , Necroptosis , Animales , Flavanonas/farmacología , Células Epiteliales/efectos de los fármacos , Células Epiteliales/virología , Células Epiteliales/metabolismo , Necroptosis/efectos de los fármacos , Apoptosis/efectos de los fármacos , Túbulos Renales/virología , Túbulos Renales/efectos de los fármacos , Túbulos Renales/citología , Túbulos Renales/patología , Potencial de la Membrana Mitocondrial/efectos de los fármacos , Antivirales/farmacología , Mitocondrias/efectos de los fármacos , Mitocondrias/metabolismo , Infecciones por Coronavirus/virología , Infecciones por Coronavirus/tratamiento farmacológico , Enfermedades de las Aves de Corral/virología , Enfermedades de las Aves de Corral/tratamiento farmacológico , Replicación Viral/efectos de los fármacos , Células CultivadasRESUMEN
With the increased awareness on food freshness and food quality among consumers, the intelligent packaging films that can visually monitor the freshness of packaged foods by observing the color changes of packaging materials are gradually drawing more and more attentions. In this paper, various colorimetric indicators, types of polysaccharides as film-forming materials, production methods, freshness monitoring application, along with the future development of different intelligent packaging films are illustrated detailedly and deeply. Natural pH sensitive indicators such as anthocyanin, alizarin, curcumin, betaines and chlorophylls, as well as the gases sensitive indicators (hydrogen sulfide sensitive indicators and ethylene sensitive indicators) are the most widely used indicators for monitoring of food freshness. By incorporating different colorimetric indicators into polysaccharides (starch, chitosan, gum and cellulose derivatives) based substrates, the intelligent packaging films can be fabricated by solvent casting method, extrusion-blow molding method and electrospinning technique for monitoring of meat products, fruits, vegetables, milk products and other food products. In conclusion, intelligent packaging films with colorimetric functions are promising and feasible methods for real-time monitoring of food freshness, while stable colorimetric indicators, new film-forming methods and cheaper polysaccharide materials are still needed to develop for further commercialization.
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Ascites syndrome (AS) in broiler chickens, also known as pulmonary arterial hypertension (PAH), is a significant disease in the poultry industry. It is a nutritional metabolic disease that is closely associated with hypoxia-inducible factors and rapid growth. The rise in pulmonary artery pressure is a crucial characteristic of AS and is instrumental in its development. Hypoxia-inducible factor 1α (HIF-1α) is an active subunit of a key transcription factor in the oxygen-sensing pathway. HIF-1α plays a vital role in oxygen homeostasis and the development of pulmonary hypertension. Studying the effects of HIF-1α on pulmonary hypertension in humans or mammals, as well as ascites in broilers, can help us understand the pathogenesis of AS. Therefore, this review aims to (1) summarize the mechanism of HIF-1α in the development of pulmonary hypertension, (2) provide theoretical significance in explaining the mechanism of HIF-1α in the development of pulmonary arterial hypertension (ascites syndrome) in broilers, and (3) establish the correlation between HIF-1α and pulmonary arterial hypertension (ascites syndrome) in broilers. HIGHLIGHTSExplains the hypoxic mechanism of HIF-1α.Linking HIF-1α to pulmonary hypertension in broilers.Explains the role of microRNAs in pulmonary arterial hypertension in broilers.
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Cell migration regulated by Thrombospondin 2 (THSB2) is important for the development of pulmonary artery remodeling, but the mechanism by which THBS2-mediated cell migration regulates the development of pulmonary artery remodeling in broiler ascites syndrome (AS) is unclear. In addition, the lack of chicken THBS2 antibodies makes it difficult to study the mechanism in depth. In our study, we used recombinant gene technology, protein purification, and other techniques to obtain mouse anti-chicken THBS2 antibody and analyze its expression in broilers, ascites broilers and other animals. The results showed that we immunized mouse with recombinant THBS2 protein and obtained an antibody titer of 1:204,800, and the addition of astragalus polysaccharide as an immunomodulator during immunization significantly increased the titer of the antibody. Western blotting (WB) and immunofluorescence results showed that the THBS2 was significantly down-regulated in the ascites broiler. The THBS2 antibody we prepared can also detect THBS2 protein in duck, mouse, goat, and rabbit tissues. These results provide a foundation for further investigation of the role of THBS2 in pulmonary artery remodeling in broiler ascites syndrome and a powerful tool for studying the role of THBS2 in AS.
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Anticuerpos , Pollos , Hipertensión Pulmonar , Proteínas Recombinantes , Trombospondinas , Animales , Proteínas Recombinantes/inmunología , Trombospondinas/inmunología , Trombospondinas/genética , Ratones , Hipertensión Pulmonar/inmunología , Anticuerpos/inmunología , Ascitis/inmunología , Arteria Pulmonar , Enfermedades de las Aves de Corral/inmunologíaRESUMEN
p62, also known as SQSTM1, has been shown to be closely related to the coronavirus. However, it remains unclear on the relationship between p62 and NIBV infection. Moreover, there are no available antibodies against the chicken p62 protein. Thus, this study aimed to prepare p62 polyclonal antibody and investigate the correlation between the p62 protein and NIBV infection. Here, PET-32a-p62 prokaryotic fusion expression vector was constructed for prokaryotic protein expression, and then p62 polyclonal antibody was prepared by immunizing rabbits. Lastly, these antibodies were then utilized in Western blotting (WB), immunohistochemistry (IHC), and immunofluorescence (IF) assays. The results showed that we successfully prepared chicken p62 polyclonal antibody. Meanwhile, WB and IF demonstrated that the expression of p62 showed a trend of first increase and then decrease after NIBV infection. IHC showed that the expression of p62 in the spleen, lung, kidney, bursa of Fabricius and trachea of chickens infected with NIBV in 11 dpi was significantly higher than that of normal chickens. Taken together, this study successfully prepared a polyclonal antibody for chicken p62 protein and confirmed its application and expression in chickens, as well as the expression of p62 in tissues after NIBV infection.
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Pollos , Infecciones por Coronavirus , Virus de la Bronquitis Infecciosa , Animales , Virus de la Bronquitis Infecciosa/inmunología , Infecciones por Coronavirus/inmunología , Infecciones por Coronavirus/virología , Enfermedades de las Aves de Corral/inmunología , Enfermedades de las Aves de Corral/virología , Proteína Sequestosoma-1/metabolismo , Proteína Sequestosoma-1/inmunología , Proteína Sequestosoma-1/genética , Anticuerpos/inmunología , Conejos , Anticuerpos Antivirales/inmunologíaRESUMEN
Yolk Peritonitis can lead to a rapid decline in egg production, which seriously affects the health of laying hens and the profitability of chicken farms. Escherichia coli (E. coli) is the most common cause of yolk peritonitis in laying hens. In this study, bacterial samples were collected from the ovaries and fallopian tubes of laying hens with suspected yolk peritonitis from a laying farm in Jiangsu Province, and their pathogenicity and drug resistance were investigated. Initially, morphological and biochemical detection methods were employed to isolate and identify the pathogenic bacteria. The results showed that a total of 16 strains of E. coli were isolated from laying hens with yolk peritonitis. Subsequently, the drug resistance and pathogenicity of a randomly selected E. coli strain were analyzed and predicted by genome sequencing technology, and the drug resistance of E. coli was verified by drug sensitivity test and PCR. Finally, the virulence was verified by infection experiment in mice. The study revealed that the egg-yolk peritonitis in laying hens was caused by E. coli infection, and the genome sequencing analysis revealed that the bacteria had multidrug resistance and high virulence. The drug susceptibility testing indicates that E. coli exhibited resistance to aminoglycosides, ß-lactam, macrolides, fluoroquinolones, and sulfonamides. In this study, resistance genes including KdpE, aadA5, APH(3 ")-ID, APH(6)-ID, and TEM-1 were identified, and their expression levels varied across different stages of bacterial growth. The results of virulence analysis indicated a mortality rate of 50% in mice infected with E. coli at a concentration of 2.985 × 107 CFU/mL. E. coli infection resulted in damage to various tissues and organs in mice, with the intestinal tissue structure being the most severely affected. This study provides a reference for the study of drug resistance mechanisms in E. coli and provides valuable insights into the selection of drugs for the treatment of vitelline peritonitis.
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Antibacterianos , Pollos , Infecciones por Escherichia coli , Escherichia coli , Peritonitis , Enfermedades de las Aves de Corral , Animales , Peritonitis/microbiología , Peritonitis/veterinaria , Peritonitis/tratamiento farmacológico , Escherichia coli/efectos de los fármacos , Escherichia coli/genética , Escherichia coli/fisiología , Escherichia coli/patogenicidad , Infecciones por Escherichia coli/veterinaria , Infecciones por Escherichia coli/microbiología , Enfermedades de las Aves de Corral/microbiología , Femenino , Antibacterianos/farmacología , Virulencia , Ratones , Farmacorresistencia Bacteriana , Yema de HuevoRESUMEN
Heavy metals interact with each other in a coexisting manner to produce complex combined toxicity to organisms. At present, the toxic effects of chronic co-exposure to heavy metals hexavalent chromium [Cr(VI)] and divalent nickel [Ni(II)] on organisms are seldom studied and the related mechanisms are poorly understood. In this study, we explored the mechanism of the colon injury in mice caused by chronic exposure to Cr or/and Ni. The results showed that, compared with the control group, Cr or/and Ni chronic exposure affected the body weight of mice, and led to infiltration of inflammatory cells in the colon, decreased the number of goblet cells, fusion of intracellular mucus particles and damaged cell structure of intestinal epithelial. In the Cr or/and Ni exposure group, the activity of nitric oxide synthase (iNOS) increased, the expression levels of MUC2 were significantly down-regulated, and those of ZO-1 and Occludin were significantly up-regulated. Interestingly, factorial analysis revealed an interaction between Cr and Ni, which was manifested as antagonistic effects on iNOS activity, ZO-1 and MUC2 mRNA expression levels. Transcriptome sequencing further revealed that the expression of genes-related to inflammation, intestinal mucus and tight junctions changed obviously. Moreover, the relative contents of Cr(VI) and Ni(II) in the Cr, Ni and Cr+Ni groups all changed with in-vitro gastrointestinal ï¼IVGï¼digestion, especially in the Cr+Ni group. Our results indicated that the chronic exposure to Cr or/and Ni can lead to damage to the mice colon, and the relative content changes of Cr(VI) and Ni(II) might be the main reason for the antagonistic effect of Cr+Ni exposure on the colon damage.
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Cromo , Colon , Mucina 2 , Níquel , Animales , Cromo/toxicidad , Níquel/toxicidad , Ratones , Colon/efectos de los fármacos , Colon/patología , Mucina 2/genética , Mucina 2/metabolismo , Óxido Nítrico Sintasa de Tipo II/metabolismo , Óxido Nítrico Sintasa de Tipo II/genética , Perfilación de la Expresión Génica , Masculino , Digestión/efectos de los fármacos , Proteína de la Zonula Occludens-1/metabolismo , Proteína de la Zonula Occludens-1/genética , Transcriptoma/efectos de los fármacos , Ocludina/metabolismo , Ocludina/genética , Mucosa Intestinal/efectos de los fármacos , Mucosa Intestinal/metabolismo , Mucosa Intestinal/patologíaRESUMEN
Long-term in situ plasma membrane-targeted imaging is highly significant for investigating specific biological processes and functions, especially for the imaging and tracking of apoptosis processes of cells. However, currently developed membrane probes are rarely utilized to monitor the in situ damage of the plasma membrane. Herein, a transition-metal complex phosphorescent indicator, Ru-Chol, effectively paired with cholesterol, exhibits excellent properties on staining the plasma membrane, with excellent antipermeability, good photostability, large Stokes shift, and long luminescence lifetime. In addition, Ru-Chol not only has the potential to differentiate cancerous cells from normal cells but also tracks in real time the entire progression of cisplatin-induced plasma membrane damage and cell apoptosis. Therefore, Ru-Chol can serve as an efficient tool for the monitoring of morphological and physiological changes in the plasma membrane, providing assistance for drug screening and early diagnosis and treatment of diseases, such as immunodeficiency, diabetes, cirrhosis, and tumors.
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Membrana Celular , Colesterol , Complejos de Coordinación , Rutenio , Humanos , Rutenio/química , Colesterol/química , Colesterol/análisis , Membrana Celular/química , Membrana Celular/metabolismo , Complejos de Coordinación/química , Complejos de Coordinación/síntesis química , Complejos de Coordinación/farmacología , Apoptosis/efectos de los fármacos , Sustancias Luminiscentes/química , Sustancias Luminiscentes/síntesis química , Cisplatino/farmacología , Antineoplásicos/farmacología , Antineoplásicos/química , Estructura MolecularRESUMEN
Luminescent ß-diketonate-europium(III) complexes have been found a wide range of applications in time-gated luminescence (TGL) bioassays, but their poor water solubility is a main problem that limits their effective uses. In this work we propose a simple and general strategy to enhance the water solubility of luminescent ß-diketonate-europium(III) complexes that permits facile synthesis and purification. By introducing the fluorinated carboxylic acid group into the structures of ß-diketone ligands, two highly water-soluble and luminescent Eu3+ complexes, PBBHD-Eu3+ and CPBBHD-Eu3+, were designed and synthesized. An excellent solubility exceeding 20 mg/mL for PBBHD-Eu3+ was found in a pure aqueous buffer, while it also displayed strong and long-lived luminescence (quantum yield φ = 26%, lifetime τ = 0.49 ms). After the carboxyl groups of PBBHD-Eu3+ were activated, the PBBHD-Eu3+-labeled streptavidin-bovine serum albumin (SA-BSA) conjugate was prepared, and successfully used for the immunoassay of human α-fetoprotein (AFP) and the imaging of an environmental pathogen Giardia lamblia under TGL mode, which demonstrated the practicability of PBBHD-Eu3+ for highly sensitive TGL bioassays. The carboxyl groups of PBBHD can also be easily derivatized with other reactive chemical groups, which enables PBBHD-Eu3+ to meet diverse requirements of biolabeling technique, to provide new opportunities for developing functional europium(III) complex biolabels serving for TGL bioassays.
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Europio , Solubilidad , Agua , Europio/química , Agua/química , Humanos , Mediciones Luminiscentes/métodos , Albúmina Sérica Bovina/química , Complejos de Coordinación/química , Complejos de Coordinación/síntesis química , Giardia lamblia/efectos de los fármacos , Luminiscencia , Animales , Bioensayo/métodos , Sustancias Luminiscentes/química , Sustancias Luminiscentes/síntesis química , Estreptavidina/química , Factores de Tiempo , Bovinos , Cetoácidos/químicaRESUMEN
Exposure to Cr and/or Ni can have widespread implications on the environment and health. However, the specific toxic effects of chronic Cr and Ni co-exposure on mice liver have not been reported. To ascertain the combined toxic effects of chronic Cr and Ni co-exposure on liver damage in mice, 80 6-week-old female C57BL/6 J mice were randomly divided into 4 groups: the Con group, Cr group (Cr+6 50 mg/L), Ni group (Ni+2 110 mg/L), and Cr + Ni group (Cr+6 50 mg/L + Ni+2 110 mg/L). The trial period lasted for 16 weeks. The results showed that Cr+6 and/or Ni+2 increased liver weight and liver index (P < 0.05) in mice, caused histological abnormality and ultrastructural damage, and micronutrients imbalance in mice liver. These findings serve as the basis for subsequent experiments. Compared with the individual exposure group, chronic Cr and Ni co-exposure resulted in decreased levels and activities of ALT, AST, MDA, T-AOC, and T-SOD (P < 0.05) in liver tissue, and decreased the mRNA expression levels of the TLR4/mTOR pathway related factors (TLR4, TRAM, TRIF, TBK-1, IRF-3, MyD88, IRAK-4, TRAF6, TAK-1, IKKß, NF-κB, IL-1ß, IL-6, TNFα, ULK1, Beclin 1, LC3) (P < 0.05) and decreased the protein expression levels of the factors (TLR4, MyD88, TRAF6, NF-κB p50, IL-6, TNFα, ULK1, LC3II/LC3I) (P < 0.05). Moreover, factorial analysis revealed the interaction between Cr and Ni, which was manifested as antagonistic effects on Cr concentration, Ni concentration, and TLR4, MyD88, NF-κB, mTOR, LC3, and p62 mRNA expression levels. In conclusion, the TLR4/mTOR pathway as a mechanism through which chronic Cr and Ni co-exposure induce liver inflammation and autophagy in mice, and there was an antagonistic effect between Cr and Ni. The above results provided a theoretical basis for understanding the underlying processes.
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Autofagia , Cromo , Inflamación , Hígado , FN-kappa B , Níquel , Transducción de Señal , Receptor Toll-Like 4 , Animales , Femenino , Ratones , Inflamación/inducido químicamente , Interleucina-6/metabolismo , Hígado/metabolismo , Ratones Endogámicos C57BL , Factor 88 de Diferenciación Mieloide/metabolismo , ARN Mensajero , Factor 6 Asociado a Receptor de TNF/metabolismo , Receptor Toll-Like 4/metabolismo , Serina-Treonina Quinasas TOR/metabolismo , Factor de Necrosis Tumoral alfa/metabolismo , Cromo/metabolismo , Cromo/toxicidad , Níquel/metabolismo , Níquel/toxicidadRESUMEN
Pulmonary artery remodeling is a characteristic feature of broiler ascites syndrome (BAS). Pulmonary artery endothelial cells (PAECs) regulated by HIF-1α play a critical role in pulmonary artery remodeling, but the underlying mechanisms of HIF-1α in BAS remain unclear. In this experiment, primary PAECs were cultured in vitro and were identified by coagulation factor VIII. After hypoxia and RNA interference, the mRNA and protein expression levels of HIF-1α and VEGF were determined by qPCR and Western blotting. The transcriptome profiles of PAECs were obtained by RNA sequencing. Our results showed that the positive rate of PAECs was more than 90%, hypoxia-induced promoted the proliferation and apoptosis of PAECs, and RNA interference significantly downregulated the expression of HIF-1α, inhibited the proliferation of PAECs, and promoted the apoptosis of PAECs. In addition, transcriptome sequencing analysis indicated that HIF-1α may regulate broiler ascites syndrome by mediating COL4A, vitronectin, vWF, ITGα8, and MKP-5 in the ECM, CAMs and MAPK pathways in PAECs. These studies lay the foundation for further exploration of the mechanisms of pulmonary artery remodeling, and HIF-1α may be a potentially effective gene for the prevention and treatment of BAS.
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Pollos , Células Endoteliales , Subunidad alfa del Factor 1 Inducible por Hipoxia , Arteria Pulmonar , Interferencia de ARN , Animales , Arteria Pulmonar/metabolismo , Arteria Pulmonar/citología , Subunidad alfa del Factor 1 Inducible por Hipoxia/genética , Subunidad alfa del Factor 1 Inducible por Hipoxia/metabolismo , Células Endoteliales/fisiología , Células Endoteliales/metabolismo , Proliferación Celular , Proteínas Aviares/genética , Proteínas Aviares/metabolismo , Enfermedades de las Aves de Corral/genética , Ascitis/veterinaria , Ascitis/genética , Apoptosis , Células CultivadasRESUMEN
The pollution and toxic effects of hexavalent chromium [Cr(VI)] and divalent nickel [Ni(II)] have become worldwide public health issues. However, the potential detailed effects of chronic combined Cr(VI) and Ni exposure on colonic inflammation in mice have not been reported. In this study, 16S rDNA sequencing, metabolomics data analysis, qPCR and other related experimental techniques were used to comprehensively explore the mechanism of toxic damage and the inflammatory response of the colon in mice under the co-toxicity of chronic hexavalent chromium and nickel. The results showed that long-term exposure to Cr(VI) and/or Ni resulted in an imbalance of trace elements in the colon of mice with significant inflammatory infiltration of tissues. Moreover, Cr(VI) and/or Ni poisoning upregulated the expression levels of IL-6, IL-18, IL-1ß, TNF-α, IFN-γ, JAK2 and STAT3 mRNA, and downregulated IL-10 mRNA, which was highly consistent with the trend in protein expression. Combined with multiomics analysis, Cr(VI) and/or Ni could change the α diversity and ß diversity of the gut microbiota and induce significant differential changes in metabolites such as Pyroglu-Glu-Lys, Val-Asp-Arg, stearidonic acid, and 20-hydroxyarachidonic acid. They are also associated with disorders of important metabolic pathways such as lipid metabolism and amino acid metabolism. Correlation analysis revealed that there was a significant correlation between gut microbes and metabolites (P < 0.05). In summary, based on the advantages of comprehensive analysis of high-throughput sequencing sets, these results suggest that chronic exposure to Cr(VI) and Ni in combination can cause microbial flora imbalances, induce metabolic disorders, and subsequently cause colonic damage in mice. These data provide new insights into the toxicology and molecular mechanisms of Cr(VI) and Ni.
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Cromo , Níquel , Animales , Ratones , Níquel/toxicidad , Cromo/análisis , Inflamación , ARN MensajeroRESUMEN
Epilepsy is a chronic neurological disorder characterized by recurrent seizures globally, imposing a substantial burden on patients and their families. The pathological role of peroxynitrite (ONOO-), which can trigger oxidative stress, inflammation, and neuronal hyperexcitability, is critical in epilepsy. However, the development of reliable, in situ, and real-time optical imaging tools to detect ONOO- in the brain encounters some challenges related to the depth of tissue penetration, background interference, optical bleaching, and spectral overlapping. To address these limitations, we present Ir-CBM, a new one-photon and two-photon excitable and long-lived ratiometric luminescent probe designed specifically for precise detection of ONOO- in epilepsy-based on the Förster resonance energy transfer mechanism by combining an iridium(III) complex with an organic fluorophore. Ir-CBM possesses the advantages of rapid response, one-/two-photon excitation, and ratiometric luminescent imaging for monitoring the cellular levels of ONOO- and evaluating the effects of different therapeutic drugs on ONOO- in the brain of an epilepsy model rat. The development and utilization of Ir-CBM offer valuable insights into the design of ratiometric luminescent probes. Furthermore, Ir-CBM serves as a rapid imaging and screening tool for antiepileptic drugs, thereby accelerating the exploration of novel antiepileptic drug screening and improving preventive and therapeutic strategies in epilepsy research.
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Epilepsia , Ácido Peroxinitroso , Humanos , Ratas , Animales , Transferencia Resonante de Energía de Fluorescencia , Iridio , Colorantes Fluorescentes , Imagen Óptica/métodos , Epilepsia/inducido químicamente , Epilepsia/diagnóstico por imagen , Encéfalo/diagnóstico por imagenRESUMEN
The adverse effects of chronic heat stress (CHS)-induced fatty liver syndrome on laying hens during the egg-producing stages have been wildly documented. However, until nowadays, the CHS responses of growing laying hens as well as its alleviating effects of vitamin C are rarely reported. In this study, 12-wk-old laying hens were subjected to CHS at 36 °C for 10 h/d for 3 wk with or without dietary supplementation of 300 mg/kg vitamin C. Results showed that CHS significantly impaired the growth performances and the liver functions of birds, as characterized by reduced feed intake and body weight, increased hepatic lipid accumulation and serum concentrations of TG, ALT, and AST, as well as the abnormal expression patterns of the lipid metabolism-related genes. Vitamin C supplementation successfully mitigated the lipid accumulation, while showing no alleviating effect on the serum contents of ALT or AST, which are two key indicators of liver functions. Metabolomic analysis based on UPLC-Q-TOF/MS identified 173 differential metabolites from the HS and HSV group samples, and they are mainly enriched in the pathways related to the cellular components, vitamin and amino acid metabolism and energy substance metabolism. The results indicate that CHS-induced hepatic lipid deposition in growing laying hens is effectively alleviated by dietary supplementation of vitamin C, which is probably resulted from the alterations of hepatocellular metabolic patterns.
Chronic heat stress (CHS)-induced fatty liver syndrome (FLS) is one of the major problems faced in poultry industry. However, the heat stress response as well as the alleviating strategies for growing laying hens is rarely concerned until nowadays. In this study, 12-wk-old laying hens were subjected to the CHS condition with or without dietary supplementation of 300 mg/kg vitamin C, we found that CHS can also remarkably impair the growth performance and liver functions and induce the hepatic lipid metabolism disorders in the growing laying hens. Vitamin C supplementation successfully mitigated the hepatic lipid accumulation, while showed no alleviating effect on the liver functions. Metabolomic analysis further identified 173 differential metabolites between CHS and HSV groups, which are mainly enriched in the pathways including the cellular components, vitamin and amino acid metabolism and the energy substance metabolism. The results suggest that vitamin C supplementation can effectively alleviate the hepatic lipid deposition in growing laying hens under CHS probably through altering their energy metabolism patterns.
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Ácido Ascórbico , Suplementos Dietéticos , Animales , Femenino , Ácido Ascórbico/farmacología , Suplementos Dietéticos/análisis , Dieta/veterinaria , Metabolismo de los Lípidos , Pollos/fisiología , Vitaminas/metabolismo , Respuesta al Choque Térmico , Hígado/metabolismo , Lípidos , Alimentación Animal/análisisRESUMEN
Nephropathogenic infectious bronchitis virus (NIBV) infections continue to pose a significant hazard in the poultry industry. Baicalin is a natural flavonoid that has been reported to have antiviral activity, but its function in NIBV infection largely remains unclear. In this study, the antiviral mechanism of baicalin in the spleen of NIBV-infected chicks was mainly elucidated in mitophagy and macrophage polarization. 28-day-old Hy-Line brown chicks were randomly divided into four groups: the group of chicks was treated intranasally (in) with normal saline (0.2 mL) and subsequently divided into two groups: the Con group (basic diet), the Con+BA group (basic diet+10 mg/kg Baicalin); another group of chicks was intranasally infected with SX9 (10-5/0.2 mL) and subsequently divided into two groups: the Dis group (basic diet), the Dis+BA group (basic diet+10 mg/kg Baicalin). Spleen tissues were collected at 3, 7, and 11 days post infection (dpi). NIBV copy number was strikingly decreased in the spleens under BA treatment with infectious time. Histopathological examination showed enlarged and hemorrhagic white pulp and no clearly defined boundary between white pulp and red pulp in the Dis group, which could be improved by BA treatment. Meanwhile, the loss of cristae structure and vacuolization in mitochondria caused by NIBV infection was repaired in the Dis+BA group by ultrastructure observation. In addition, BA treatment inhibited the induction of mitophagy by NIBV infection. BA treatment also promoted innate immunity by enhancing type I IFN levels. Moreover, BA treatment up-regulated M1-related cytokines (iNOS, TNF-α, IL-1ß, IL-6) and inhibited M2-related cytokines (ARG2, IL-4, IL-10, Pparg) at the mRNA and protein levels. However, the results from the splenic tissues at 11 dpi are opposite results from 3 and 7 dpi. Immunofluorescence analysis for M1 macrophage marker iNOS and M2 macrophage marker CD163 further validated this result. Collectively, BA inhibited mitophagy and triggered IFN activation, and M1 polarization, which contributed to the inhibition of NIBV infection.
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Virus de la Bronquitis Infecciosa , Animales , Bazo , Mitofagia , Pollos , Flavonoides/farmacología , Citocinas/genética , Macrófagos , AntiviralesRESUMEN
Beclin1, also known as ATG6, has been shown to be closely related to coronavirus, however, the link between Beclin1 and nephropathogenic infectious bronchitis virus (NIBV) has been poorly investigated and there are no available antibodies specifically targeting the chicken Beclin1 protein. The study aimed to prepare and assay a polyclonal antibody to Beclin1, enabling a deeper understanding of the mechanism of action of Beclin1 in NIBV. In this study, we amplified the chicken Beclin1 target gene and constructed a recombinant plasmid using prokaryotic expression techniques, then obtained the recombinant target protein by induced expression. Finally, the serum is obtained by immunizing rabbits with the purified and concentrated protein. The results show that the antiserum potency of the ELISA assay was >1:204800. By western blotting and immunofluorescence, the antibodies we prepared specifically recognized the chicken Beclin1 protein, which is mainly found in the nucleus of trachea, lung, kidney, spleen and fabricant cells. NIBV infection significantly decreased the expression of Beclin1 in the trachea, but increased in others. We have successfully prepared specific rabbit anti-chicken Beclin1 polyclonal antibodies, and detected changes in tissues of diseased chickens infected with NIBV, laying the foundation for further studies on the role of Beclin1 in avian diseases.
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Pollos , Virus de la Bronquitis Infecciosa , Animales , Conejos , Virus de la Bronquitis Infecciosa/genética , Beclina-1/genética , Beclina-1/metabolismo , Anticuerpos , Riñón/metabolismo , Western BlottingRESUMEN
This study aimed to understand the changes in the milk and gut microbiota of dairy cows with mastitis, and to further explore the relationship between mastitis and the microbiota. In this study, we extracted microbial DNA from healthy and mastitis cows and performed high-throughput sequencing using the Illumina NovaSeq sequencing platform. OTU clustering was performed to analyze complexity, multi-sample comparisons, differences in community structure between groups, and differential analysis of species composition and abundance. The results showed that there were differences in microbial diversity and community composition in the milk and feces of normal and mastitis cows, where the diversity of microbiota decreased and species abundance increased in the mastitis group. There was a significant difference in the flora composition of the two groups of samples (P < 0.05), especially at the genus level, the difference in the milk samples was Sphingomonas (P < 0.05) and Stenotrophomonas (P < 0.05), the differences in stool samples were Alistipes (P < 0.05), Flavonifractor (P < 0.05), Agathobacter (P < 0.05) and Pygmaiobacter (P < 0.05). In conclusion, the microbiota of the udder and intestinal tissues of dairy cows suffering from mastitis will change significantly. This suggests that the development of mastitis is related to the endogenous pathway of microbial intestinal mammary glands, but the mechanisms involved need further study.
Asunto(s)
Lactobacillales , Mastitis , Microbiota , Femenino , Bovinos , Animales , Humanos , Leche , ADN Ribosómico/genética , Secuenciación de Nucleótidos de Alto RendimientoRESUMEN
It is well established that PRRSV elimination is an effective strategy for PRRS control, but published reports concerning successful PRRSV elimination cases in farrow-to-finishing herds are rare. Here, we have reported a successful PRRSV elimination case in a farrow-to-finish herd by employing a "herd closure and rollover" approach with some modifications. Briefly, the introduction of pigs to the herd was stopped and normal production processes were maintained until the herd reached a PRRSV provisional negative status. During the herd closure, strict biosecurity protocols were implemented to prevent transmission between nursery pigs and sows. In the current case, introducing gilts before herd closure and live PRRSV exposure were skipped. In the 23rd week post-outbreak, the pre-weaning piglets started to show 100% PRRSV negativity in qPCR tests. In the 27th week, nursery and fattening barns fully launched depopulation. In the 28th week, nursery and fattening houses reopened and sentinel gilts were introduced into gestation barns. Sixty days post-sentinel gilt introduction, the sentinel pigs maintained being PRRSV antibody negative, manifesting that the herd matched the standard of the provisional negative status. The production performance of the herd took 5 months to bounce back to normal. Overall, the current study provided additional information for PRRSV elimination in farrow-to-finish pig herds.
Asunto(s)
Síndrome Respiratorio y de la Reproducción Porcina , Virus del Síndrome Respiratorio y Reproductivo Porcino , Enfermedades de los Porcinos , Porcinos , Animales , Femenino , Virus del Síndrome Respiratorio y Reproductivo Porcino/genética , Síndrome Respiratorio y de la Reproducción Porcina/prevención & control , Sus scrofa , DesteteRESUMEN
Copper (Cu) can be harmful to host physiology at high levels, although it is still unclear exactly how it causes nephrotoxicity. Mitochondrial dysfunction and endoplasmic reticulum (ER) stress are associated with heavy metal intoxication. Meanwhile, mitochondria and ER are connected via mitochondria-associated ER membranes (MAM). In order to reveal the crosstalk between them, a total of 144 1-day-old Peking ducks were randomly divided into four groups: control (basal diet), 100 mg/kg Cu, 200 mg/kg Cu, and 400 mg/kg Cu groups. Results found that excessive Cu disrupted MAM integrity, reduced the co-localization of IP3R and VDAC1, and significantly changed the MAM-related factors levels (Grp75, Mfn2, IP3R, MCU, PACS2, and VDAC1), leading to MAM dysfunction. We further found that Cu exposure induced mitochondrial dysfunction via decreasing the ATP level and the expression levels of COX4, TOM20, SIRT1, and OPA1 and up-regulating Parkin expression level. Meanwhile, Cu exposure dramatically increased the expression levels of Grp78, CRT, and ATF4, resulting in ER stress. Overall, these findings demonstrated MAM plays the critical role in Cu-induced kidney mitochondrial dysfunction and ER stress, which deepened our understanding of Cu-induced nephrotoxicity.
Asunto(s)
Cobre , Patos , Animales , Cobre/toxicidad , Cobre/metabolismo , Retículo Endoplásmico/metabolismo , Mitocondrias/metabolismo , Riñón/metabolismo , Estrés del Retículo EndoplásmicoRESUMEN
Excessive vanadium (V) contamination is an attracting growing concern, which can negatively affect the health of human and ecosystems. But how V causes nephrotoxicity and the role of mitochondria-associated endoplasmic reticulum membrane (MAM) in V-induced nephrotoxicity have remained elusive. To explore the detailed mechanism and screen of potential effective drugs for V-evoked nephrotoxicity, a total of 72 ducks were divided into two groups, control group and V group (30 mg/kg V). Results showed that excessive V damaged kidney function of ducks including causing histopathological abnormality, biochemical makers derangement and oxidative stress. Then MAM of duck kidneys was extracted to investigate differentially expressed proteins (DEPs) under V exposure using proteomics analysis. Around 4240 MAM-localized proteins were identified, of which 412 DEPs showed dramatic changes, including 335 upregulated and 77 downregulated DEPs. On the basis of gene ontology (GO), string and KEGG database analysis, excessive V led to nephrotoxicity primarily by affecting MAM-mediated metabolic pathways, especially elevating the endoplasmic Reticulum (ER) proteostasis related pathway. Further validation analysis of the detected genes and proteins of ER proteostasis related pathway under V poisoning revealed a consistent relationship with proteome analysis, indicating that V disrupted MAM-mediated ER proteostasis. Accordingly, our data proved the critical role for MAM in V-evoked nephrotoxicity, particularly with MAM-mediated ER proteostasis, providing promising insights into the toxicological exploration mechanisms of V.