通过调节脂多糖诱导的急性肺损伤(ALI)中的TRAF6-c-Myc信号通路,鱼腥草素钠可减轻铁变态反应。

IF 2.8 3区 医学 Q2 PHARMACOLOGY & PHARMACY
Juan Li, Yan-Ping Hu, Xing-Ling Liang, Ming-Wei Liu
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引用次数: 0

摘要

人们已经广泛研究了鱼腥草钠(SH)对脂多糖(LPS)诱导的 ALI 的影响。然而,铁突变是否参与了这一过程仍不明确。本研究旨在找出 SH 对 LPS 诱导的铁蛋白沉积的影响和可能机制。用 LPS 处理大鼠 ALI 模型和 II 型肺泡上皮(ATII)细胞损伤模型。通过酶联免疫吸附试验(ELISA)、苏木精-伊红(HE)染色和吉氏染色来确定 SH 对 LPS 诱导的 ALI 的影响。此外,透射电子显微镜、细胞计数试剂盒-8(CCK8)、亚铁比色试剂盒、免疫组织化学、免疫荧光、活性氧试剂盒、Western 印迹(Wb)和 qRT-PCR 检测了 SH 对 LPS 诱导的铁变态反应和铁变态反应相关通路的影响。结果发现,使用 SH 处理可抑制 LPS 诱导的铁蛋白沉积,从而显著减轻 ALI。铁变态反应表现为谷胱甘肽过氧化物酶 4(GPX4)、FTH1 和谷胱甘肽(GSH)水平的下降,丙二醛(MDA)、活性氧(ROS)、NOX1、NCOA4 和 Fe2+ 的积累以及线粒体结构的破坏。SH通过调节TRAF6-c-Myc抑制了ALI大鼠和大鼠ATII细胞的铁突变。研究结果表明,SH治疗可通过抑制铁细胞凋亡减轻LPS诱导的ALI,其作用模式与体内和体外调节TRAF6-c-Myc信号通路有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sodium Houttuyniae attenuates ferroptosis by regulating TRAF6-c-Myc signaling pathways in lipopolysaccharide-induced acute lung injury (ALI).

The impact of Sodium Houttuyniae (SH) on lipopolysaccharide (LPS)-induced ALI has been investigated extensively. However, it remains ambiguous whether ferroptosis participates in this process. This study aimed to find out the impacts and probable mechanisms of SH on LPS-induced ferroptosis. A rat ALI model and type II alveolar epithelial (ATII) cell injury model were treated with LPS. Enzyme-linked immunosorbent assay (ELISA), hematoxylin-eosin (HE) staining, and Giemsa staining were executed to ascertain the effects of SH on LPS-induced ALI. Moreover, Transmission electron microscopy, Cell Counting Kit-8 (CCK8), ferrous iron colorimetric assay kit, Immunohistochemistry, Immunofluorescence, Reactive oxygen species assay kit, western blotting (Wb), and qRT-PCR examined the impacts of SH on LPS-induced ferroptosis and ferroptosis-related pathways. Theresults found that by using SH treatment, there was a remarkable attenuation of ALI by suppressing LPS-induced ferroptosis. Ferroptosis was demonstrated by a decline in the levels of glutathione peroxidase 4 (GPX4), FTH1, and glutathione (GSH) and a surge in the accumulation of malondialdehyde (MDA), reactive oxygen species (ROS), NOX1, NCOA4, and Fe2+, and disruption of mitochondrial structure, which were reversed by SH treatment. SH suppressed ferroptosis by regulating TRAF6-c-Myc in ALI rats and rat ATII cells. The results suggested that SH treatment attenuated LPS-induced ALI by repressing ferroptosis, and the mode of action can be linked to regulating the TRAF6-c-Myc signaling pathway in vivo and in vitro.

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来源期刊
BMC Pharmacology & Toxicology
BMC Pharmacology & Toxicology PHARMACOLOGY & PHARMACYTOXICOLOGY&nb-TOXICOLOGY
CiteScore
4.80
自引率
0.00%
发文量
87
审稿时长
12 weeks
期刊介绍: BMC Pharmacology and Toxicology is an open access, peer-reviewed journal that considers articles on all aspects of chemically defined therapeutic and toxic agents. The journal welcomes submissions from all fields of experimental and clinical pharmacology including clinical trials and toxicology.
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