Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6
Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6
复制标题
GSS 通过 TNF-α 和 IL-6 对脂多糖诱导的内皮细胞损伤和 ALI 的抑制作用
DOI：
10.1155/2019/4251394
复制
发表时间：
2019-12-30
影响因子：
4.6
通讯作者：
Huan, Jingning
中科院分区：
文献类型：
--
作者：
Yi, Lei;Zhou, Zengding;Huan, Jingning
背景脓毒症条件下，LPS诱导肺血管内皮细胞（EC）损伤，炎症介质的释放启动并加重急性肺损伤（ALI）。对于ALI没有有效的治疗选择。染料木黄酮-3 '-磺酸钠（Genistein-3 '-sodium sulfonate，GSS）是天然大豆黄酮的衍生物，具有抗细胞凋亡的作用.然而，GSS是否保护对脓毒症引起的EC损伤和炎症介质的释放尚未确定。本研究发现，GSS不仅在体内下调小鼠肺和血清中TNF-α和IL-6的水平，而且还抑制EC中TNF-α和IL-6的表达和分泌。重要的是，我们还发现GSS通过Myd 88/NF-κ B信号通路阻断LPS诱导的EC中TNF-α和IL-6的表达。综上所述，我们的研究结果表明，GSS可能是一个有前途的候选人脓毒症诱导的ALI通过其调节肺EC的炎症反应。
Background. Under septic conditions, LPS induced lung vascular endothelial cell (EC) injury, and the release of inflammatory mediator launches and aggravates acute lung injury (ALI). There are no effective therapeutic options for ALI. Genistein-3 '-sodium sulfonate (GSS) is a derivative of native soy isoflavone, which exhibits neuroprotective effects via its antiapoptosis property. However, whether GSS protect against sepsis-induced EC injury and release of inflammatory mediators has not been determined. In this study, we found that GSS not only downregulated the levels of TNF-alpha and IL-6 in the lung and serum of mice in vivo but also inhibited the expression and secretion of TNF-alpha and IL-6 in ECs. Importantly, we also found that GSS blocked LPS-induced TNF-alpha and IL-6 expression in ECs via the Myd88/NF-kappa B signaling pathway. Taken together, our results demonstrated that GSS might be a promising candidate for sepsis-induced ALI via its regulating effects on inflammatory response in lung ECs.