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首页> 外文期刊>International immunopharmacology >Anomalin attenuates LPS-induced acute lungs injury through inhibition of AP-1 signaling
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Anomalin attenuates LPS-induced acute lungs injury through inhibition of AP-1 signaling

机译：异常通过抑制AP-1信号传导衰减LPS诱导的急性肺损伤

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In the present study, the anomalin was investigated to determine the protective effects and underlying mechanism against LPS-induced acute lung injury in mice. Anomalin administration 30 min after the LPS injection, significantly attenuated the mechanical allodynia, decrease body temperature, and improved the histological changes and inhibited the infiltration of leukocytes. The anomalin treatment markedly inhibited the production of pro-inflammatory mediators such as cytokines (IL-1 beta, IL-6 and TNF-alpha) and NO in contrast to the LPS treated groups. Similarly, the anomalin also enhanced the level of anti-oxidant enzymes such as GST, GSH, Catalase and inhibited oxidative stress marker such as MDA. In order to explore the molecular mechanism the effect of anomalin was evaluated for mitogen activated protein kinases (MAPK) in US-stimulated RAW264.7 cells. The anomalin treatment significantly attenuated the MAPK proteins such as ERK1/2, JNK and p38 (which is downstream signaling proteins to the MAPKKKs and MAPKKs protein) in the RAW264.7 macrophages using western blot analysis. Furthermore, the western blot analysis showed that anomalin treatment significantly inhibited the activation of the Akt proteins in the RAW264.7 macrophages. The AP-1 served as downstream target for the MAPK pathways and the blocking MAPK pathways is responsible for the inhibition of the AP-1 protein. The AP-1/DNA binding was assessed in the RAW264.7 cells using EMSA. The anomalin treatment significantly restricted the AP-1/DNA binding activity and the decrease in the AP-1/DNA binding activity might be contributed due to the upstream inhibition of the MAPKs signaling.
机译：在本研究中，研究了异常，以确定对小鼠急性肺损伤的保护作用和潜在机制。在LPS注射后30分钟的异常给药，显着减弱机械异常，减少体温，并改善组织学变化，抑制白细胞的渗透。异常治疗显着抑制了促炎介质的产生，例如细胞因子（IL-1β，IL-6和TNF-α），与LPS处理基团相比没有。类似地，异常也增强了抗氧化酶的水平，例如GST，GSH，过氧化氢酶和抑制氧化应激标记，例如MDA。为了探讨分子机制，在美国刺激的Raw264.7细胞中对丝裂原激活蛋白激酶（MAPK）评估了异常的作用。使用Western印迹分析，异常治疗显着衰减了MAPK蛋白如ERK1 / 2，JNK和P38（在Mapkkkks和MapKkks和Mapkkks蛋白中）。此外，Western印迹分析表明，异常治疗显着抑制Raw264.7巨噬细胞中Akt蛋白的激活。 AP-1用作MAPK途径的下游靶标，阻断MAPK途径负责抑制AP-1蛋白。使用EMSA在Raw264.7细胞中评估AP-1 / DNA结合。异常治疗显着地限制了AP-1 / DNA结合活性，并且由于MAPK信号传导的上游抑制，可以促进AP-1 / DNA结合活性的降低。

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