nuclear factor kappa light chain enhancer of activated B cells
Gliclazide reduced oxidative stress, inflammation, and bone loss in an experimental periodontal disease model.
The purpose of this study was to evaluate the effect of gliclazide on oxidative stress, inflammation, and bone loss in experimental periodontal disease model.Male albino Wistar rats were divided into no binder, binder, and a ligature with 1, 5, and 10 mg / kg of gliclazide group , Maxillary fixed and scanned using micro-computed tomography to measure linear and bone volume / tissue volume (BV / TV) and volumetric bone loss.
Histopathology, the analysis of immunohistochemistry and immunofluorescence performed to test the matrix metalloproteinase-2 (MMP-2), cyclooxygenase 2 (COX-2), cathepsin K, member activator receptor nuclear factor kappa-Β ligand (RANKL), an activator receptor nuclear factor kappa-Β (RANK), osteoprotegerin (OPG) pathway, the migration of macrophage inhibitory factor (MIF), superoxide dismutase-1 (SOD-1), glutathione peroxidase-1 (GPx-1), NFkB p 50 (cytoplasm), NLS NFkB p50 (signal nuclear localization), PI3 kinase and AKT staining. Myeloperoxidase activity, malondialdehyde and glutathione levels, while interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) levels were evaluated by ultraviolet-visible spectroscopy analysis.
A reverse transcription quantitative polymerase chain reaction was used to measure gene expression of nuclear factor kappa B subunit p50 (NF-kB p50), phosphoinositide 3-kinase (PI3K), protein kinase B (AKT) and F4 / 80.Micro tomography -computed showed that 1 mg / kg of gliclazide treatment reduces bone loss is linear compared with a ligature, 5 mg / kg of gliclazide, and 10 mg / kg of gliclazide treatment.
All concentrations of gliclazide increase bone volume / tissue volume (BV / TV) compared with a binder. Treatment with 1 mg / kg of gliclazide reduce myeloperoxidase activity, malondialdehyde, IL-1β and TNF-α levels (P ≤ 0.05), and results in weak staining for COX-2, cathepsin K, MMP-2, RANK, RANKL , -1 SOD, GPx-1, MIF and PI3K. Furthermore, down-regulation of NF-kB p50, PI3K, Akt, and F4 / 80 were observed, and OPG strong staining after treatment 1 mg / kg of gliclazide treatment.This decreased migration of neutrophils and macrophages, decreased inflammatory response, and decreased bone loss in rats with ligature-induced periodontitis.
Gliclazide reduced oxidative stress, inflammation, and bone loss in an experimental periodontal disease model.
Preventing gliclazide 5-FU-Induced Oral Mucositis by Reducing Oxidative Stress, Inflammation, and P-Selectin Adhesion Molecules.
Oral mucositis (OM) is one of the main side effects of the treatment of head and neck cancers, particularly radiotherapy and / or chemotherapy. OM is characterized by ulcers, erythema, dysphagia, xerostomia, and increased susceptibility to opportunistic infections. In the perspective of finding a pharmacological therapy to prevent inflammation and ulceration of the OM, the investigation of the pleiotropic effects of commercial drugs are needed, including gliclazide, antidiabetic drugs.
This study aimed to evaluate the effect of gliclazide in experimental models of OM induced by 5-fluorouracil. male hamster pre-treated with oral gliclazide (1, 5, or 10 mg / kg) for 10 days. Cheek pouch samples were subjected to histopathological and immunohistochemical analysis (COX2, iNOS, MMP-2, NF P65, GPx) and imunofluorescence (P-selectin). IL-1β and TNF-α levels, Myeloperoxidase activity (MPO) and the level of malondialdehyde (MDA) was investigated by ultraviolet-visible spectroscopy analysis.
Description: A polyclonal antibody against NFKB1. Recognizes NFKB1 from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: WB, IHC, ELISA;WB:1/500-1/2000.IHC:1/100-1/300.ELISA:1/20000
Description: A polyclonal antibody against NFKB1. Recognizes NFKB1 from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: IHC, ELISA;IHC:1/100-1/300.ELISA:1/5000
Description: A polyclonal antibody against NFKB1. Recognizes NFKB1 from Human. This antibody is Unconjugated. Tested in the following application: WB, IHC, ELISA;WB:1/500-1/2000.IHC:1/100-1/300.ELISA:1/20000
Description: A polyclonal antibody against NFKB1. Recognizes NFKB1 from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: WB, IHC, ELISA;WB:1/500-1/2000.IHC:1/100-1/300.ELISA:1/20000
Description: A polyclonal antibody against NFKB1. Recognizes NFKB1 from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: ELISA, WB
Description: A polyclonal antibody against NFKB1. Recognizes NFKB1 from Human. This antibody is Unconjugated. Tested in the following application: WB, ELISA;WB:1/500-1/2000.ELISA:1/20000
Description: A polyclonal antibody against NFKB1. Recognizes NFKB1 from Human. This antibody is Unconjugated. Tested in the following application: WB, IHC, IP, ELISA;WB:1/500-1/2000.IHC:1/100-1/300.IP:2-5ug/mglysate.ELISA:1/10000
Description: A polyclonal antibody against NFKB1. Recognizes NFKB1 from Human, Mouse. 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:1/40000
Description: A polyclonal antibody against NFKB1. Recognizes NFKB1 from Human, Mouse. 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:1/40000
Description: A polyclonal antibody against NFKB1. Recognizes NFKB1 from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: ELISA, IHC;ELISA:1:500-1:5000, IHC:1:5-1:20
Description: A polyclonal antibody against NFKB1. Recognizes NFKB1 from Human. This antibody is Unconjugated. Tested in the following application: ELISA, WB, IHC, IF, ChIP; Recommended dilution: WB:1:500-1:5000, IHC:1:100-1:500, IF:1:50-1:500
Description: A polyclonal antibody against NFKB1. Recognizes NFKB1 from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: ELISA, WB;ELISA:1:1000-1:2000, WB:1:200-1:1000
Description: A polyclonal antibody against NFKB1. Recognizes NFKB1 from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: ELISA, IHC;ELISA:1:500-1:5000, IHC:1:25-1:100
Description: This gene encodes a 105 kD protein which can undergo cotranslational processing by the 26S proteasome to produce a 50 kD protein. The 105 kD protein is a Rel protein-specific transcription inhibitor and the 50 kD protein is a DNA binding subunit of the NF-kappa-B (NFKB) protein complex. NFKB is a transcription regulator that is activated by various intra- and extra-cellular stimuli such as cytokines, oxidant-free radicals, ultraviolet irradiation, and bacterial or viral products. Activated NFKB translocates into the nucleus and stimulates the expression of genes involved in a wide variety of biological functions. Inappropriate activation of NFKB has been associated with a number of inflammatory diseases while persistent inhibition of NFKB leads to inappropriate immune cell development or delayed cell growth. Two transcript variants encoding different isoforms have been found for this gene.
Description: NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. [UniProt]
Description: NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52 and the heterodimeric p65-p50 complex appears to be most abundant one. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NFkB is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NFkB complexes are held in the cytoplasm in an inactive state complexed with members of the NFkB inhibitor (I-kappa-B) family. In a conventional activation pathway, IkB is phosphorylated by IkB kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NFkB complex which translocates to the nucleus. NF-kappa-B heterodimeric p65-p50 and RelB-p50 complexes are transcriptional activators. The NFkB p50-p50 homodimer is a transcriptional repressor, but can act as a transcriptional activator when associated with BCL3. NFKB1 appears to have dual functions such as cytoplasmic retention of attached NFkB proteins by p105 and generation of p50 by a cotranslational processing. The proteasome-mediated process ensures the production of both p50 and p105 and preserves their independent function, although processing of NFKB1/p105 also appears to occur post-translationally. p50 binds to the kappa-B consensus sequence 5'-GGRNNYYCC-3', located in the enhancer region of genes involved in immune response and acute phase reactions. In a complex with MAP3K8, NFKB1/p105 represses MAP3K8-induced MAPK signaling; active MAP3K8 is released by proteasome-dependent degradation of NFKB1/p105.
Description: Nuclear factor NF-kappa-B p105/p50, also called EBP-1 is a protein that in humans is encoded by the NFKB1 gene. By fluorescence in situ hybridization, the gene was assigned to human chromosome 4q24. NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NFKB1 appears to have dual functions such as cytoplasmic retention of attached NF-kappa-B proteins by p105 and generation of p50 by a cotranslational processing.
Description: This gene encodes a 105 kD protein which can undergo cotranslational processing by the 26S proteasome to produce a 50 kD protein. The 105 kD protein is a Rel protein-specific transcription inhibitor and the 50 kD protein is a DNA binding subunit of the NF-kappa-B (NFKB) protein complex. NFKB is a transcription regulator that is activated by various intra- and extra-cellular stimuli such as cytokines, oxidant-free radicals, ultraviolet irradiation, and bacterial or viral products. Activated NFKB translocates into the nucleus and stimulates the expression of genes involved in a wide variety of biological functions. Inappropriate activation of NFKB has been associated with a number of inflammatory diseases while persistent inhibition of NFKB leads to inappropriate immune cell development or delayed cell growth. Two transcript variants encoding different isoforms have been found for this gene.
Description: NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52 and the heterodimeric p65-p50 complex appears to be most abundant one. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NFkB is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NFkB complexes are held in the cytoplasm in an inactive state complexed with members of the NFkB inhibitor (I-kappa-B) family. In a conventional activation pathway, IkB is phosphorylated by IkB kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NFkB complex which translocates to the nucleus. NF-kappa-B heterodimeric p65-p50 and RelB-p50 complexes are transcriptional activators. The NFkB p50-p50 homodimer is a transcriptional repressor, but can act as a transcriptional activator when associated with BCL3. NFKB1 appears to have dual functions such as cytoplasmic retention of attached NFkB proteins by p105 and generation of p50 by a cotranslational processing. The proteasome-mediated process ensures the production of both p50 and p105 and preserves their independent function, although processing of NFKB1/p105 also appears to occur post-translationally. p50 binds to the kappa-B consensus sequence 5'-GGRNNYYCC-3', located in the enhancer region of genes involved in immune response and acute phase reactions. In a complex with MAP3K8, NFKB1/p105 represses MAP3K8-induced MAPK signaling; active MAP3K8 is released by proteasome-dependent degradation of NFKB1/p105.
NLS NF P50 protein levels were analyzed by western blotting. The group treated with gliclazide at a dose of 10 mg / kg showed the presence of erythema, there was no evidence of erosion, and the absence of mucosal ulceration with a score of 1 (1-2) (p <0.01).
