Lenvatinib is known that NF B in the cytoplasm and the limits I B as an inactive

E that NF B in a DSS-induced colitis is enabled. Zun Highest our Lenvatinib results showed that DSS treatment strongly induced I B phosphorylation and degradation loan St as I Similar results were also obtained by Zingarelli et al. and Song et al. Second, the expression of phospho NF B p65, which was as a marker for NF-activation was regulated significantly after the treatment of DSS. It is known that NF B in the cytoplasm and the limits I B as an inactive complex. Phosphorylation and degradation of IB result in the separation of the complex, so NF B is activated and transported to the nucleus, where it can induce gene transcription by binding to specific promoter elements. Therefore, subsequent The degradation of protein phosphorylation and I B important events for NF B activation, suggesting that NF B is activated and translocated into the nucleus.
Therefore, NF B will be an ideal target for therapy of ulcerative colitis. For this reason, considerable efforts have been made to Including new treatments Lich the use of medicinal plants or their active components targeting NF as develop parthenolide, an active ingredient in the plant feverfew traditionally used for various diseases since ancient times and today is used clinically to treat in the treatment of a number of diseases in China, has recently been shown to be an inhibitor of NF B-powerful activation and inhibit effective k can TheDamage. This is an insidious cycle. If this vicious cycle is not interrupted, the inflammatory response strengths to develop and verst.
It is therefore very important for effective treatment of the CPU to interrupt this vicious circle. In this cycle plays an NF B The key, as it controlled The production of IL 1 and TNF. Therefore k nnte The blockade of NF B have entered a dinner break in the feedback loop. In fact, the most established drugs already in UC as cortico Of sulfasalazine and are known for their anti-inflammatory known about mediated inhibition of NF-B activity t . In addition, local treatment leads to NF B decoy oligonucleotides or NF B p65 antisense oligonucleotides to an improvement in chronic experimental colitis in M Mice due to decreased production of entzndungsf Accompanied facilitative cytokines.
In Similar way in our current data also demonstrated that administration of parthenolide not only NF-B activity t reduces but also reduces the accumulation of leukocytes, downregulated IL-1 and TNF-production in the inflammatory response, and hence improved fa Significantly, the severity of DSS-induced colitis. To play a lot of inflammatory mediators such as IL-1, TNF, COX-2, iNOS and adhesion Apply sion molecule as an R What is essential in the inflammatory process of UC. Therefore, blocking these inflammatory mediators offer an alternative therapy for UC. However, it is insufficient to achieve the optimal therapeutic effect to block individual factors multifactorial disease such as UC. In fact, the individual factor as a cytokine molecule or the candidate is a downstream target, w During NF B is the final common pathway or limiting step in the inflammatory cascade. Obviously, as a therapeutic target, h Lt NF B a big promise it. Therefore, in order

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