This study was conducted to determine the effect of food Scenedesmus ovalternus on growth and resistance to disease Gibel carp (Carassius gibelio) during overwintering. Gibel carp (initial weight: 90.39 ± 0.33 g) were fed with diets containing 0% or 4% Scenedesmus ovalternus (DS0 and DS4) for 4 weeks during the period of overwintering early, and then all the fish were left unfed during the period of overwintering end. A challenge test using the bacteria Aeromonas hydrophila then done.
4% Scenedesmus ovalternus diet had no effect on the growth of Gibel carp (P> 0.05), but did not increase the survival rate after challenge (P ≤ 0.05). In the DS0 group, the challenge of decreasing bacterial content of complement 3 (C3), immunoglobulin M (IgM), interleukin 2 (IL2) and tumor necrosis factor α (TNF) in fish (P <0.05); in the group DS4, the challenge of increasing the total antioxidant capacity (T-AOC) and myeloperoxidase (MPO) activity but decreased the content of IL2 and TNF (P <0.05). MPO activity and content C3, IgM and TNFa was higher in the group was given a diet DS4 from DS0 after bacterial challenge (P <0.05).
Compared with the pre-challenge, the level of expression of toll like receptor 2 (TLR2), Toll like receptor 3 (TLR3), Toll like receptor 4 (TLR4), differentiation factors myeloid 88 (MyD88), Toll / IL-1 receptor domain-containing protein adapter (Tirap), TIR-domain-containing adapter-inducing interferon-β (Trif), nuclear factor kappa polypeptide enhancer genes of light in B-cells inhibitor of α (IκBα), transforming growth factor β (TGFβ), interleukin 1β (IL1β) tumor necrosis factor α1 (TNFα1) and interleukin 10 (IL-10) in the head kidney Gibel carp induced after challenge (P <0.05). Gibel carp fed a diet DS4 showed lower expression of TGFβ in the head kidney prior to challenge and lower expression of TLR2, TLR3, TLR4, Tirap, Trif, IκBα, TNFα1, IL-10 and TGFβ after a challenge from the feed DS0 diet ( P <0.05). Overall, ovalternus Scenedesmus supplements increase the resistance of Gibel carp of the A. hydrophila after overwintering through TLR signaling pathway.
Dietary Scenedesmus ovalternus improves disease resistance of overwintering gibel carp (Carassius gibelio) by alleviating toll-like receptor signaling activation.
NF-kB dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Cells Tissue Culture.
Dimeric transcription factor NF-kB regulates many cellular response pathways, including pathways to induce the expression of inflammatory cytokines and chemokines. Constitutive NF-kB and proteins sequestered in the cytosol by inhibition of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα). NF-kB activation requires IκBα degradation, which then exposes the nuclear localization signal on NF-kB and promote trade to the core. Once in the nucleus, NF-kB binding to the promoter region of the gene targets of NF-kB as interleukin 6 (IL-6) and IL-23 to promote their expression. Activation of NF-kB occurs independently of transcription or translation.
Description: This gene encodes a member of the NF-kappa-B inhibitor family, which contain multiple ankrin repeat domains. The encoded protein interacts with REL dimers to inhibit NF-kappa-B/REL complexes which are involved in inflammatory responses. The encoded protein moves between the cytoplasm and the nucleus via a nuclear localization signal and CRM1-mediated nuclear export. Mutations in this gene have been found in ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant disease.
Description: This gene encodes a member of the NF-kappa-B inhibitor family, which contain multiple ankrin repeat domains. The encoded protein interacts with REL dimers to inhibit NF-kappa-B/REL complexes which are involved in inflammatory responses. The encoded protein moves between the cytoplasm and the nucleus via a nuclear localization signal and CRM1-mediated nuclear export. Mutations in this gene have been found in ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant disease.
Description: This gene encodes a member of the NF-kappa-B inhibitor family, which contain multiple ankrin repeat domains. The encoded protein interacts with REL dimers to inhibit NF-kappa-B/REL complexes which are involved in inflammatory responses. The encoded protein moves between the cytoplasm and the nucleus via a nuclear localization signal and CRM1-mediated nuclear export. Mutations in this gene have been found in ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant disease.
Description: A polyclonal antibody against Phospho-FOS (S32). Recognizes Phospho-FOS (S32) from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: WB, ELISA;WB:1/500-1/2000.ELISA:1/5000
Description: A polyclonal antibody against Phospho-NFKBIA (S32/S36). Recognizes Phospho-NFKBIA (S32/S36) from Human, Mouse, Rat, Monkey. This antibody is Unconjugated. Tested in the following application: WB, IHC, IF, ELISA;WB:1/500-1/2000.IHC:1/100-1/300.IF:1/200-1/1000.ELISA:1/10000
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human Phospho-BAD(S32) . This antibody is tested and proven to work in the following applications:
Description: This gene encodes a member of the NF-kappa-B inhibitor family, which contain multiple ankrin repeat domains. The encoded protein interacts with REL dimers to inhibit NF-kappa-B/REL complexes which are involved in inflammatory responses. The encoded protein moves between the cytoplasm and the nucleus via a nuclear localization signal and CRM1-mediated nuclear export. Mutations in this gene have been found in ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant disease.
Description: This gene encodes a member of the NF-kappa-B inhibitor family, which contain multiple ankrin repeat domains. The encoded protein interacts with REL dimers to inhibit NF-kappa-B/REL complexes which are involved in inflammatory responses. The encoded protein moves between the cytoplasm and the nucleus via a nuclear localization signal and CRM1-mediated nuclear export. Mutations in this gene have been found in ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant disease.
Description: This gene encodes a member of the NF-kappa-B inhibitor family, which contain multiple ankrin repeat domains. The encoded protein interacts with REL dimers to inhibit NF-kappa-B/REL complexes which are involved in inflammatory responses. The encoded protein moves between the cytoplasm and the nucleus via a nuclear localization signal and CRM1-mediated nuclear export. Mutations in this gene have been found in ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant disease.
Description: Immunofluorescence staining of A549 cells with CSB-RA015761A32phHU at 1:100,counter-stained with DAPI. The cells were fixed in 4% formaldehyde, permeabilized using 0.2% Triton X-100 and blocked in 10% normal Goat Serum. The cells were then incubated with the antibody overnight at 4℃. The secondary antibody was Alexa Fluor 488-congugated AffiniPure Goat Anti-Rabbit IgG (H+L).
Description: Immunofluorescence staining of A549 cells with CSB-RA015761A32phHU at 1:100,counter-stained with DAPI. The cells were fixed in 4% formaldehyde, permeabilized using 0.2% Triton X-100 and blocked in 10% normal Goat Serum. The cells were then incubated with the antibody overnight at 4℃. The secondary antibody was Alexa Fluor 488-congugated AffiniPure Goat Anti-Rabbit IgG (H+L).
Rabbit anti-T7 IgG, primary antibody, Conjugated to Alkaline Phosphatase
Description: This gene encodes a member of the NF-kappa-B inhibitor family, which contain multiple ankrin repeat domains. The encoded protein interacts with REL dimers to inhibit NF-kappa-B/REL complexes which are involved in inflammatory responses. The encoded protein moves between the cytoplasm and the nucleus via a nuclear localization signal and CRM1-mediated nuclear export. Mutations in this gene have been found in ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant disease.
×
Therefore, the activation of NF-kB country should be measured either by measuring NF-kB specifically in the nucleus, or by measuring the expression of NF-kB target genes. In this protocol, the cells were stably transfected with the NF-kB :: luciferase reporter construct were tested for activation of NF-kB in vitro using tissue culture techniques. These cells are infected with Salmonella Typhimurium to activate NF-kB, the traffic to the nucleus and binds to kB sites in the promoter region of luciferase, induces the expression. Cells lysed and analyzed by luciferase assay system. The amount of luciferase produced by the cells correlated with the intensity of the luminescence signal, which is detected by reader.t plate
