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首页> 外文期刊>Cellular Physiology and Biochemistry >Escin Increases the Survival Rate of LPS-Induced Septic Mice Through Inhibition of HMGB1 Release from Macrophages
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Escin Increases the Survival Rate of LPS-Induced Septic Mice Through Inhibition of HMGB1 Release from Macrophages

机译：Escin通过抑制巨噬细胞释放HMGB1来提高LPS诱导的败血症小鼠的存活率。

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Background: Previous studies have described the effects of Escin on improving the survival rate of endotoxemic animals. The purpose of this study was to explore the molecular mechanisms of this potentially beneficial treatment. Methods: First, the survival rate of endotoxemic mice was monitored for up to 2 weeks after Escin pretreatment, Escin post-treatment, or Escin post-treatment + rHMGB1. The effects of Escin on the release of pro-inflammatory cytokines such as TNF-α, IL-1β, IL-6 and HMGB1 in the serum of endotoxemic mice and LPS-induced macrophages were evaluated by ELISA. Furthermore, the mRNA and protein levels of HMGB1 in LPS-induced macrophages were measured by qRT-PCR and Western blot, respectively. Additionally, the release of pro-inflammatory cytokines such as TNF-α, IL-1β, IL-6 was evaluated by ELISA in rHMGB1-induced macrophages. Finally, the protein levels and the activity of NF-κB in macrophages were checked by Western blot and ELISA, respectively. Results: Both pretreatment and post-treatment with Escin could improve the survival rate of endotoxemic mice, while exogenous rHMGB1 reversed this effect. In addition, Escin decreased the level of the pro-inflammatory cytokines TNF-α, IL-1β, IL-6 and HMGB1 in endotoxemic mice and in LPS-induced macrophages. Escin could also inhibit the mRNA levels and activity of HMGB1. The release of the pro-inflammatory cytokines TNF-α, IL-1β, IL-6 could be suppressed in rHMGB1-induced macrophages by Escin. Finally, Escin could suppress the activation of NF-κB in LPS-induced macrophages. Conclusion: Escin could improve the survival of mice with LPS-induced endotoxemia. This effect maybe meditated by reducing the release of HMGB1, resulting in the suppression of the release of pro-inflammatory cytokines.
机译：背景：先前的研究已经描述了Escin对提高内毒素动物的存活率的作用。这项研究的目的是探讨这种潜在有益治疗的分子机制。方法：首先，监测内毒素血症小鼠在Escin预处理，Escin后处理或Escin后处理+ rHMGB1后长达2周的存活率。通过ELISA评估Escin对内毒素血症小鼠和LPS诱导的巨噬细胞血清中促炎性细胞因子如TNF-α，IL-1β，IL-6和HMGB1释放的影响。此外，分别通过qRT-PCR和Western blot检测LPS诱导的巨噬细胞中HMGB1的mRNA和蛋白水平。另外，通过ELISA在rHMGB1诱导的巨噬细胞中评估促炎细胞因子如TNF-α，IL-1β，IL-6的释放。最后，分别通过蛋白质印迹和ELISA检测巨噬细胞中的蛋白质水平和NF-κB活性。结果：Escin预处理和后处理均可提高内毒素血症小鼠的存活率，而外源性rHMGB1可逆转此效应。此外，Escin降低了内毒素血症小鼠和LPS诱导的巨噬细胞中促炎性细胞因子TNF-α，IL-1β，IL-6和HMGB1的水平。 Escin还可以抑制HMGB1的mRNA水平和活性。 Escin可以抑制rHMGB1诱导的巨噬细胞中促炎细胞因子TNF-α，IL-1β，IL-6的释放。最后，Escin可以抑制LPS诱导的巨噬细胞中NF-κB的活化。结论：Escin可以改善LPS致内毒素血症小鼠的存活率。可以通过减少HMGB1的释放来抑制这种作用，从而抑制促炎性细胞因子的释放。

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