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首页> 外文期刊>Digestive Diseases and Sciences >Ischemic Preconditioning-Induced SOCS-1 Protects Rat Intestinal Ischemia Reperfusion Injury via Degradation of TRAF6
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Ischemic Preconditioning-Induced SOCS-1 Protects Rat Intestinal Ischemia Reperfusion Injury via Degradation of TRAF6

机译:缺血预处理诱导的SOCS-1保护大鼠肠缺血再灌注损伤通过TRAF6的降解保护

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摘要

The inflammatory immune response plays an important role in mesenteric ischemia and ischemia-reperfusion injury. Toll-like receptor 4 (TLR4) is a critical receptor in transduction of the inflammatory response and plays an important role in intestinal homeostasis. Tumor necrosis factor receptor-associated factor 6 (TRAF6), known as a key adaptor protein downstream of TLR4, is involved in the inflammatory response by activating multiple apoptotic signaling pathways. However, mechanisms of the suppressor of cytokine signaling-1 (SOCS-1) in regulating cell inflammation and apoptosis are still obscure.
机译:炎症免疫反应在肠系膜缺血和缺血再灌注损伤中起重要作用。 Toll样受体4(TLR4)是转导炎症反应的关键受体,并在肠道稳态中起重要作用。 肿瘤坏死因子受体相关因子6(TRAF6),称为TLR4下游的关键适配器蛋白,通过激活多次凋亡信号传导途径参与炎症反应。 然而,细胞因子信号传导-1(SoCS-1)在调节细胞炎症和细胞凋亡中的抑制剂的机制仍然模糊不清。

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