ArticleBMC pharmacology & toxicology2024
Sodium Houttuyniae attenuates ferroptosis by regulating TRAF6-c-Myc signaling pathways in lipopolysaccharide-induced acute lung injury (ALI).
Article in BMC pharmacology & toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Crosstalk between microRNA and oxidative stress in ovarian cancer: diagnosis, pathogenesis and therapeutic resistance.Medical oncology (Northwood, London, England) · 2025Review
- Siji Kangbingdu Mixture Ameliorates LPS-Induced Acute Lung Injury by Downregulating the TNF/IL-17 Signaling Pathways: A Comprehensive Study Using Transcriptomics, Network Pharmacology and Experimental Verification.Journal of inflammation research · 2025Article
- Bioinformatics Identification and Validation of Ferroptosis-Related Key Genes and Therapeutic Compounds in Septic Lung Injury.Journal of inflammation research · 2024Article
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4 authors.
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Abstract
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 Fe
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