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Lipopolysaccharide induced MAP kinase activation in RAW 264.7 cells attenuated by cerium oxide nanoparticles

机译:脂多糖诱导被氧化铈纳米粒子减弱的RAW 264.7细胞中的MAP激酶激活

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摘要

High mortality rates are associated with the life threatening disease of sepsis. Improvements in septic patient survivability have failed to materialize with currently available treatments. This article represents data regarding a study published in biomaterials (Vellaisamy et al., Biomaterials, 2015, in press). with the purpose of evaluating whether severe sepsis mortality and associated hepatic dysfunction induced by lipopolysaccharide (LPS) can be prevented by cerium oxide nanoparticles (CeO2NPs) treatment in male Sprague Dawley rats. Here we provide the information about the method and processing of raw data related to our study publish in Biomaterials and Data in Brief (Vellaisamy et al., Biomaterials, 2015, in press; Vellaisamy et al., Data in Brief, 2015, in press.). The data contained in this article evaluates the contribution of MAPK signaling in LPS induced sepsis. Macrophage cells (RAW 264.7) were treated with a range of cerium oxide nanoparticle concentration in the presence and absence of LPS. Immunoblotting was performed on the cell lysates to evaluate the effect of cerium oxide nanoparticle treatment on LPS induced changes in Mitogen Activated Protein Kinases (MAPK) p-38, ERK 1/2, and SAPK/JNK phosphorylation.
机译:高死亡率与脓毒症威胁生命的疾病有关。败血症患者生存能力的改善无法通过当前可用的治疗方法实现。本文表示有关发表在生物材料上的一项研究的数据(Vellaisamy等人,Biomaterials,2015年,印刷中)。目的评估氧化铈纳米颗粒(CeO2NPs)治疗雄性Sprague Dawley大鼠是否可以预防脂多糖(LPS)诱导的严重败血症死亡率和相关的肝功能障碍。在此,我们提供有关与研究相关的原始数据的方法和处理的信息,这些研究和数据发表在《生物材料和数据简报》中(Vellaisamy等人,Biomaterials,2015年,印刷中; Vellaisamy等人,Data in Brief,2015年,印刷中)。本文包含的数据评估了LAPK诱导的败血症中MAPK信号传导的作用。在存在和不存在LPS的情况下,用一定范围的氧化铈纳米颗粒浓度处理巨噬细胞(RAW 264.7)。对细胞裂解物进行了免疫印迹,以评估氧化铈纳米粒子处理对LPS诱导的丝裂原活化蛋白激酶(MAPK)p-38,ERK 1/2和SAPK / JNK磷酸化变化的影响。

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