A regulation of nuclear factor kappa B (NF-kB) is a transcription protein cellular modulators of biological activity through binding to the promoter region of the nucleus and copying various protein gene. Recent studies have involved intensive role of nuclear factor kappa B (NF-kB) in diseases such as autoimmune disorders, inflammatory, cardiovascular and neurodegenerative diseases.
Therefore, targeting the nuclear factor kappa B (NF-kB) offers new opportunities protein as a therapeutic approach. Activation of IκB kinase / NF-kB signaling pathway leads to the development of a variety of pathological conditions in humans, such as neurodegenerative, inflammatory disorders, autoimmune diseases and cancer.
Therefore, the transcriptional activity of IκB kinase / NF-kB are very organized in various lines cascade. Nuclear factor NF-kB pathway plays a major role in the expression of pro-inflammatory genes including cytokines, chemokines, and adhesion molecules. In response to diverse stimuli, exiled cytosolic NF-kB in an inactive form by binding to a protein molecule inhibitor (IKB) are phosphorylated and translocated to the nucleus of the transcript about the different genes required to modify various cellular functions.
Various studies confirm the role of different protein family members of the NF-kB is involved in the expression of various gene products and mediate various cellular cascades. MicroRNAs, as a regulator of NF kB microRNAs play an important role in the regulation of inflammatory processes. Therefore, inhibitors of NF-kB and family members play a new therapeutic target in preventing various diseases. Regulation of NF kB signaling pathway may be a treatment strategy that is safe and effective for various disorders.
Role of Nuclear factor kappa B (NF-κB) Signalling in Neurodegenerative Diseases: An Mechanistic Approach.
Relieves asiaticoside Cerebral Ischemia-Reperfusion Injury through nod2 / mitogen-Activated Protein Kinase (MAPK) / Nuclear Factor kappa B (NF-kB) Signaling Pathway.
BACKGROUND Cerebral ischemia-reperfusion injury (FEATURE) is still a serious health problem. Centella formulations used to treat central nervous system disorders. In this study, asiaticoside, extracts from plants Centella asiatica, FEATURES investigated in vivo and in vitro. MATERIALS AND METHODS We modeled in vivo in mice FEATURES SD treated by middle cerebral artery occlusion, and cell models of ischemia-reperfusion injury was made in PC12 cells treated by a lack of oxygen and glucose / restoration. FEATURE vivo was assessed with a score of neurologic function, encephaledema, and the area of cerebral infarction.
levels of inflammation and oxidative stress levels that are detected by the appropriate kit. TUNEL assay was performed to assess cell apoptosis and Western blot analysis was performed to assess the level of protein expression. CCK8 assay was performed to evaluate cell viability and flow cytometer is used to detect cell apoptosis in vitro.
RESULTS function of nerve injury, brain edema, cell apoptosis, infarct size, apoptosis- related protein expression and protein expression of nod2 / MAPK / NF-kappaB signaling pathway in the model MARKS all reversed by asiaticoside in rats. The apoptotic cells, the levels of inflammation and oxidative stress levels in models of ischemia-reperfusion injury to the brain is reduced asiaticoside. Effect of asiaticoside on FEATURE inverted by NOD-2 agonists.
Description: LDLR (low density lipoprotein receptor) is a member of the LDL receptor gene family, which includes LDLR, LRP, Megalin, VLDLR, and ApoER2. The LDL receptor family is characterized by a cluster of cysteine-rich class A repeats, epidermal growth factor (EGF)-like repeats, YWTD repeats, and an O-linked sugar domain. The LDL receptor is a cell surface transmembrane protein that mediates the uptake of low density lipoprotein and its degradation in the lysosome, which provides cholesterol to cells. The cytoplasmic domain of the LDL receptor is necessary for the receptor to cluster in coated pits, which promotes the rapid endocytosis of bound LDL. Mutations in LDLR cause the autosomal dominant disease, familial hypercholesterolemia (FH), which promotes premature coronary atherosclerosis.
Description: Intracellular channel that mediates calcium release from the endoplasmic reticulum following stimulation by inositol 1,4,5-trisphosphate. Involved in the regulation of epithelial secretion of electrolytes and fluid through the interaction with AHCYL1. Plays a role in ER stress-induced apoptosis. Cytoplasmic calcium released from the ER triggers apoptosis by the activation of CaM kinase II, eventually leading to the activation of downstream apoptosis pathways.
Description: The very-low-density-lipoprotein receptor (VLDLR) is a transmembrane lipoprotein receptor of the low-density-lipoprotein (LDL) receptor family. VLDLR shows considerable homology with the members of this lineage. Discovered in 1992 by T. Yamamoto, VLDLR is widely distributed throughout the tissues of the body, including the heart, skeletal muscle, adipose tissue, and the brain, but is absent from the liver. This receptor has an important role in cholesterol uptake, metabolism of apolipoprotein E-containing triacylglycerol-rich lipoproteins, and neuronal migration in the developing brain. In humans, VLDLR is encoded by the VLDLR gene. Mutations of this gene may lead to a variety of symptoms and diseases, which include type I lissencephaly, cerebellar hypoplasia, and atherosclerosis.
Description: Receptor for granulocyte colony-stimulating factor (CSF3), essential for granulocytic maturation. Plays a crucial role in the proliferation, differientation and survival of cells along the neutrophilic lineage. In addition it may function in some adhesion or recognition events at the cell surface. Mutations in CSF3R acquired in multipotent hematopoietic progenitor cells and resulting in truncated hyper-responsive forms of the receptor, have been identified in most cases of severe congenital neutropenia (SCN). Patients carrying these mutations are at risk for developing myelodysplastic syndromes and/or acute myeloid leukemia. Constitutive mutations leading to hyporesponsive forms of the receptor are responsible for the refractoriness to CSF3 treatment observed in some SCN patients.
Description: Mouse polyclonal to Chemokine Receptor D6
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CONCLUSION Asiaticoside shown a protective effect against ischemia-reperfusion injury of the brain through nod2 / MAPK / NF-kappaB signaling pathway. These findings are particularly important for future research on the use of asiaticoside in MARKS, providing a new way to reduce FEATURES.
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 
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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