TIPE2 ameliorates neuroinflammation and cognitive impairment in sepsis-associated encephalopathy through regulating RhoA/ROCK2–NF-κB signaling pathway
Min YuanGuoqing JingQian KongTingqian MingJing ZuoQian WangYong FengWanhong LiuXiaojing WuZhongyuan Xia
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PubMed search was performed using the key words: NF-?B, nuclear factors, asthma. Articles were selected based on their relevance to this review.To review the literature regarding the involvement of the nuclear factor kappa-B (NF-?B) transcription factor in asthma.NF-?B is a critical transcription factor for the production of many inflammatory cytokines. NF-?B is associated with several diseases, including asthma, where there is an inflammation of the airways with cell infiltration. It is activated in bronchial asthmatic patient biopsies and active in the epithelium of the airways in mice after stimulation. It also participates in the maintenance of the chronic inflammatory response. NF-?B also acts synergistically with other transcription factors, to induce the maximal expression of genes involved with asthma. Activation of NF- ?B by several stimuli induces the release and degradation of the inhibitory protein I-?B from the dimeric complex followed by translocation of NF-?B to the nucleus.The NF-?B pathway is central to the pathogenesis of asthma. NF?B is an important therapeutic target for the treatment of asthma, including intermediate products on the signaling pathway and protein related to Rel. Alterations in the NF-?B signaling pathway are associated with the disease.
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In un-stimulated cells, transcription factor NF-κB is kept in cytoplasm through interaction with IκB inhibitory proteins. Exposure to inducers stimuli results in IκB phosphorylation and ubiquitilation. Liberated NF-κB is trans-located to the nucleus and bind to DNA, where they regulate the expression of a wide variety of genes. Recent studies have indicated that the NF-κB plays a central role in the regulation of inflammatory diseases and the study of the regulation of NF-κB pathways will provide a platform for developing specific therapy for inflammatory diseases.
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IL-4 plays a pivotal role in the development of the Th2 cell mediated humoral immune response and causes IgE-dependent allergic inflammatory diseases. Expression of IL-4 in differentiated Th2 cells is regulated by transcription factors such as NF-AT, AP-1 and NF-IL6. Recently, increasing evidence indicates that the pro-inflammatory transcription factor NF-kappa B may also participate inIL-4 expression. In this study, we show that the IL-4 promoter is synergistically activated by NF-kappa B, NF-AT and NF-IL6 at the NF-kappa B/NF-AT/NF-IL6 composite sites. In addition, we performed the chromatin immunoprecipitation technique to determine the functional relevance of NF-kappa B in the activation of the IL-4 gene in vivo. We demonstrate that NF-kappa B binds to the IL-4 promoter in vivo upon T cell activation. Inhibition of NF-kappa B nuclear translocation in living cells blocked binding of NF-kappa B to the IL-4 promoter. The data provide first evidence that NF-kappa B is directly involved in IL-4 transcription.
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The inducible transcription factor nuclear factor-kappa B (NF-kappaB) plays a central role in regulation of many immune, inflammatory and carcinogenic responses. While normal activation of NF-kappaB is required for cell survival and immunity, aberrant regulation of NF-kappaB leads to development of many pathological states especially those involved in acute inflammation. Recent advances in our knowledge of the signaling mechanisms those control the activation of NF-kappaB highlights the intriguing aspect of NF-kappaB regulation, namely the ability of many different signal transduction pathways originating from a wide variety of inducing mechanisms to converge on a single target, the NF-kappaB/IkappaB complex. In this review we summarize our current understanding of the NF-kappaB signaling pathways, their role in various cellular responses and the potential of using NF-kappaB as a therapeutic target in modern medicine.
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Osteoarthritis (OA) is a common joint illness that negatively impacts people's lives. The main active ingredient of cassia seed or rhubarb is chrysophanol, which acts as a SIRT6 activator. It has various pharmacological effects including anticancer, anti-diabetes and blood lipid regulation. Previous evidence suggests that chrysophanol has anti-inflammatory properties in various diseases, but its effect on OA has not been investigated yet. In this study, chrysophanol inhibited IL-1β -induced expression of ADAMTS-4, MMP13, COX-2 and iNOS. Meanwhile, it can inhibit aggrecan and collagen degradation in osteoarthritic chondrocytes induced by IL-1β.Further studies depicted that SIRT6 silencing eliminated the chrysophanol effect on IL-1β. The results demonstrated that chrysophanol could stimulate SIRT6 activation and, more importantly, increase SIRT6 levels. We also discovered that chrysophanol might impede the NF-κB pathway of OA mice’s chondrocytes induced by IL-1β, which could be because it depends on SIRT6 activation to some extent. It had also been previously covered that chrysophanol could produce a marked effect on Nrf2/NF-κB axis[1]. Therefore, we can infer that chrysophanol may benefit chondrocytes by regulating the SIRT6/NF-κB and Nrf2/NF-κB signaling axis.We examined the anti-inflammatory mechanism and the impact of chrysophanol on mice in vitro and in vivo. In summary, we declare that chrysophanol diminishes the inflammatory reaction of OA in mice in vitro by regulating SIRT6/NF-κB and Nrf2/NF-κB signaling pathway and protects articular cartilage from degradation in vivo. We can infer that chrysophanol could be an efficient therapy for OA.
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