nuclear factor kappa light chain enhancer of activated B cells
Pipoxolan suppresses the inflammatory factors of NF-κB, AP-1, and STATs, but activates the antioxidative factor Nrf2 in LPS-stimulated RAW 264.7 murine macrophage cells
Although pipoxolan (PIPO) is a smooth muscle relaxant, anti-inflammatory abilities have not been studied. Therefore, we investigated the molecular mechanism of anti-inflammatory PIPO in lipopolysaccharide (LPS) -induced RAW 264.7 macrophages. In this study, we used the MTT assay to evaluate cytotoxicity of the applied enzyme-linked immunosorbent assay to determine the inflammatory cytokines, and performed Western blotting to assess protein expression.
The results showed that PIPO significantly inhibited the production of cytokines, including nitric oxide, prostaglandin E2, tumor necrosis factor-α and interleukin-6. PIPO also suppresses pro-inflammatory mediator expression with inducible nitric oxide synthase and cyclooxygenase-2. Additionally, PIPO forbidden lane transcription factor of inflammatory several, including the inhibitor of kappa B / nuclear factor of κ chain enhancer light B cells (NF-kB), mitogen-activated protein kinase / activator protein-1 (AP-1),
Janus kinase / signal transducer and activator of transcription (STAT), and pulses like receptor 4 (TLR4) / serine / threonine kinase (Akt). In addition, effective PIPO activated nuclear factor erythroid 2-related factor 2 (Nrf2) / heme oxygenase-1 antioxidant pathway. Collectively, PIPO may attenuate the inflammatory effects through affecting LPS / TLR4 receptor binding; suppress the expression of anti-inflammatory transcription factor NF-kB, AP-1 and STAT; and activate the transcription factor Nrf2 antioxidant in LPS-stimulated RAW 264.7 mouse cells.
Pipoxolan suppresses the inflammatory factors of NF-κB, AP-1, and STATs, but activates the antioxidative factor Nrf2 in LPS-stimulated RAW 264.7 murine macrophage cells
Rhaponticin the effects of oxidative stress and inflammation in the diabetic retina through NRF2 / HO-1 / NF-kB signaling
Oxidative stress and inflammation has long been considered responsible for the development and progression of diabetic retinopathy. On the other hand, rhaponticin (RN) has received scientific attention for its wide range of pharmacological properties. Keeping all this in view, this study was conducted to investigate the potential protective effect of RN to the retina in diabetic rats. Rats were randomly divided into three groups: a control group of mice, rats diabetic groups, diabetes + RN (20 mg / kg body weight for 28 days via the oral route) mice groups. RN supplementation to significantly prevent diabetic mice lose weight reduction end, weekly fasting reduced blood glucose levels and HbA1c levels with a significant increase in serum levels of insulin.
Quantitative polymerase chain reaction and immunohistochemical analysis found increased regulation of Nrf2, NQO-1, HO-1 and upregulation of genes Keap1 and distribution of protein along with a significant level reduces malondialdehyde and increased activity of superoxide dismutase, catalase, and glutathione peroxidase in diabetes RN-treated mice compared to diabetic rats. In addition, treatment of diabetic mice with RN showed downregulated the expression of tumor necrosis factor-α, matrix metalloproteinase-2 and upregulated the expression of interleukin-10 (IL-10) and TIMP-1 in the retina. RN treatment decreased nuclear factor kappa-light-chain-enhancer of activated B cells and increased distribution of IL-10 protein distribution in the retina of diabetic rats. In addition, the RN treatment improved morphological changes were observed in the retina of diabetic rats.
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. The heterodimeric RELA-NFKB1 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. The NF-kappa-B heterodimeric RELA-NFKB1 and RELA-REL complexes, for instance, function as transcriptional activators. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. The inhibitory effect of I-kappa-B on NF-kappa-B through retention in the cytoplasm is exerted primarily through the interaction with RELA. RELA shows a weak DNA-binding site which could contribute directly to DNA binding in the NF-kappa-B complex. Beside its activity as a direct transcriptional activator, it is also able to modulate promoters accessibility to transcription factors and thereby indirectly regulate gene expression. Associates with chromatin at the NF-kappa-B promoter region via association with DDX1. Essential for cytokine gene expression in T-cell.
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. In unstimulated cells, NF-κB is sequestered in the cytoplasm by IκB inhibitory proteins. NF-κB-activating agents can induce the phosphorylation of IκB proteins, targeting them for rapid degradation through the ubiquitin-proteasome pathway and releasing NF-κB to enter the nucleus where it regulates gene expression.
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. In unstimulated cells, NF-κB is sequestered in the cytoplasm by IκB inhibitory proteins. NF-κB-activating agents can induce the phosphorylation of IκB proteins, targeting them for rapid degradation through the ubiquitin-proteasome pathway and releasing NF-κB to enter the nucleus where it regulates gene expression.
Description: NF-kappa-B is a ubiquitous transcription factor involved in several biological processes. It is held in the cytoplasm in an inactive state by specific inhibitors. Upon degradation of the inhibitor| NF-kappa-B moves to the nucleus and activates transcription of specific genes. NF-kappa-B is composed of NFKB1 or NFKB2 bound to either REL| RELA| or RELB. The most abundant form of NF-kappa-B is NFKB1 complexed with the product of this gene| RELA. Four transcript variants encoding different isoforms have been found for this gene.
Description: NF-kappa-B is a ubiquitous transcription factor involved in several biological processes. It is held in the cytoplasm in an inactive state by specific inhibitors. Upon degradation of the inhibitor| NF-kappa-B moves to the nucleus and activates transcription of specific genes. NF-kappa-B is composed of NFKB1 or NFKB2 bound to either REL| RELA| or RELB. The most abundant form of NF-kappa-B is NFKB1 complexed with the product of this gene| RELA. Four transcript variants encoding different isoforms have been found for this gene.
Description: NF-kappa-B is a ubiquitous transcription factor involved in several biological processes. It is held in the cytoplasm in an inactive state by specific inhibitors. Upon degradation of the inhibitor| NF-kappa-B moves to the nucleus and activates transcription of specific genes. NF-kappa-B is composed of NFKB1 or NFKB2 bound to either REL| RELA| or RELB. The most abundant form of NF-kappa-B is NFKB1 complexed with the product of this gene| RELA. Four transcript variants encoding different isoforms have been found for this gene.
Overall, these results provide clear evidence that treatment of diabetic rats with diabetic retinal changes RN attenuated through hypoglycemic, antioxidant and anti-inflammatory effects. Prolonged inflammatory response can lead to the development of from some chronic diseases, such as autoimmune disorders and the development of from natural therapeutic agent needed. A murine model was used to assess the effects of anti-inflammatory from the glucoside megastigmane, icariside B 2 (ICS B ), and the assessment was carried out in vitro , and in vivo.
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