Baicalin Inhibits Cell Proliferation and Inflammatory Cytokines Induced by Tumor Necrosis Factor α (TNF-α) in Human Immortalized Keratinocytes (HaCaT) Human Keratinocytes by Inhibiting the STAT3/Nuclear Factor kappa B (NF-κB) Signaling Pathway.
BACKGROUND quercetin (Que) reported to induce apoptosis of lung cancer cells. Src is closely related to the development of lung cancer is non-small cell (NSCLC) and can be affected by Que in macrophages. In this study, the interaction between Que and Src signaling in NSCLC cell NSCLC explored to explain the anti-function Que.
MATERIALS AND METHODS HCC827 NSCLC cell lines were subjected to administration of Que at different concentrations. Que influence on tumor cell proliferation was detected using MTT and colony formation test. Then the effect on the migration and invasion ability was assessed using the initial and Transwell test. At the molecular level, changes in Src / Fn14 / NF-kappaB signaling is determined using western blotting tests.
The role of Src in Que function further explored by inducing the expression of Src gene in NSCLC cells prior to administration Que. The test results were verified in vitro using a mouse model of NSCLC. RESULTS Que inhibits the proliferation and anchorage-independent cell growth in NSCLC. Additionally, Que delayed in closing a gap in the level of initial tests and a decrease in the number of cells in the membrane-penetrating Transwell test. At the molecular level, Que suppressed the expression of Src, which then inhibit Fn14 / NF-kappaB signaling.
In in vivo tests, Que inhibits the growth of solid tumors. After the excess of Src in NSCLC cells, the effect of anti-NSCLC NSCLC Que blocked by inducing the proliferation and metastasis, and by activating Fn14 / NF-kappaB signaling. In addition, the induced levels of Src promoted the growth and metastatic potential of solid tumors in mice. CONCLUSION Que anti-NSCLC given effect by inhibiting Src-mediated Fn14 / NF-kappaB pathway both in vitro and in vivo.
Baicalin Inhibits Cell Proliferation and Inflammatory Cytokines Induced by Tumor Necrosis Factor α (TNF-α) in Human Immortalized Keratinocytes (HaCaT) Human Keratinocytes by Inhibiting the STAT3/Nuclear Factor kappa B (NF-κB) Signaling Pathway.
Osteoarthritis Prevented in Mice by Verbascoside via Nuclear Factor kappa B (NF-kB) Downregulation Pathway.
BACKGROUND Cartilage degeneration for osteoarthritis (OA), the most adversely affects the quality of life by inhibiting the movement. This study investigated the verbascoside role in the protection of cartilage degeneration caused by osteoarthritis. MATERIALS AND METHODS enzyme-linked immunosorbent assay (ELISA) and western blot test is used to determine the secretion of inflammatory cytokines in serum and cartilage tissue, respectively.
RESULTS Treatment of the mice with excess verbascoside OA inhibiting interleukin (IL) -6, tumor necrosis factor (TNF) -alpha, and IL-1SS in serum and cartilage tissue.
P2X7R expression and matrix metalloproteinase (MMP) -13 is much higher in mice induced by OA. However, the administration reversed verbascoside OA-induced upregulation of P2X7R and MMP-13 expression in cartilage tissue. OA-mediated increase in substance P (SP) and prostaglandin E2 (PGE2) expression was also reduced in cartilage tissue by verbascoside treatment. Western blot assay revealed that treatment verbascoside IkappaBalpha markedly decreased activation of NF-kappaB and p65 in mice OA.
CONCLUSION So, verbascoside inhibits the secretion of inflammatory cytokines in rats OA by targeting P2X7R expression, the production of matrix metalloproteinases, PGE2 and downregulation of NF-kappaB signaling pathway. Therefore, verbascoside can be used as an effective agent for the treatment of osteoarthritis.
The Onco-suppressor p53 is a transcription factor that regulates a broad spectrum of genes involved in various cellular functions including apoptosis, cell cycle arrest, senescence, autophagy, DNA repair and angiogenesis. p53 and NF-kB generally has the opposite effect on the cancer cells.
Description: Anti-Kappa recognizes surface immunoglobulin on normal and neoplastic B-cells, and has been indicated as a potential aid in the identification of leukemias, plasmacytomas, and certain non-Hodgkin's lymphomas, where the expression of a single light chain class is restricted. The determination of light chain ratio is critical in evaluating B-cell neoplasms, as the majority of B-cell lymphomas express either kappa or lambda light chains, while a mixture of kappa and lambda is characteristic of reactive proliferations. In paraffin-embedded tissue, Anti-Kappa displays strong staining of kappa-positive plasma cells, as well as cells that have absorbed exogenous immunoglobulins.
Description: IkappaB beta is a protein encoded by the NFKBIB gene which is approximately 37,7 kDa. IkappaB beta is localised to the cytoplasm and nucleus. It is involved in activated TLR4 signalling, toll-like receptor signalling pathways and the 4-1BB pathway. This protein falls under the NF-kappa-B inhibitor family, which inhibits NF-kappa-B by complexing with it and trapping it in the cytoplasm. Phosphorylation of serine residues on the protein marks it for destruction via the ubiquitination pathway, thereby allowing activation of the NF-kappa-B, which then translocates to the nucleus to function as a transcription factor. IkappaB beta is expressed in the liver, lung, pancreas, nervous system and blood. STJ97539 was developed from clone 1F3 and was affinity-purified from mouse ascites by affinity-chromatography using specific immunogen. This primary antibody detects endogenous levels of IkappaB beta.
Description: IkappaB-alpha is a protein encoded by the NFKBIA gene which is approximately 35,6 kDa. IkappaB-alpha is localised to the cytoplasm and nucleus. It is involved in activated TLR4 signalling, the TNFR1 pathway, 4-1BB pathway and toll-like receptor signalling pathways. This protein falls under the NF-kappa-B inhibitor family. It inhibits the activity of dimeric NF-kappa-B/REL complexes by trapping REL dimers in the cytoplasm through masking of their nuclear localization signals. On cellular stimulation by immune and proinflammatory responses it becomes phosphorylated promoting ubiquitination and degradation, enabling the dimeric RELA to translocate to the nucleus and activate transcription. IkappaB-alpha is expressed in adherent monocytes. Mutations in the NFKBIA gene may result in ectodermal dysplasia and leukorrhea. STJ93782 was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen. This polyclonal antibody detects endogenous levels of IkappaB-alpha protein.
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Antibodies | Assay Kits | Biology Cells | cDNA | Clia Kits | Culture Cells | Devices | DNA | DNA Templates | DNA Testing | Elisa Kits | Enzymes | Equipments | Exosomes | Gels | Isotypes | Medium & Serums | NATtrol | Panel | Particles | PCR | Pcr Kits | Peptides | Reagents | Recombinant Proteins | Ria Kits | RNA | Test Kits | Uncategorized | Vector & Virus | Western Blot 
Antibodies | Assay Kits | Biology Cells | cDNA | Clia Kits | Culture Cells | Devices | DNA | DNA Templates | DNA Testing | Elisa Kits | Enzymes | Equipments | Exosomes | Gels | Isotypes | Medium & Serums | NATtrol | Panel | Particles | PCR | Pcr Kits | Peptides | Reagents | Recombinant Proteins | Ria Kits | RNA | Test Kits | Uncategorized | Vector & Virus | Western Blot 
Antibodies | Assay Kits | Biology Cells | cDNA | Clia Kits | Culture Cells | Devices | DNA | DNA Templates | DNA Testing | Elisa Kits | Enzymes | Equipments | Exosomes | Gels | Isotypes | Medium & Serums | NATtrol | Panel | Particles | PCR | Pcr Kits | Peptides | Reagents | Recombinant Proteins | Ria Kits | RNA | Test Kits | Uncategorized | Vector & Virus | Western Blot
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