ArticleYonsei medical journal2021
Effect and Mechanism Study of Sodium Houttuyfonate on Ventilator-Induced Lung Injury by Inhibiting ROS and Inflammation.
Article in Yonsei medical journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 9 citations in OpenAlex.
- Sodium Houttuyniae attenuates ferroptosis by regulating TRAF6-c-Myc signaling pathways in lipopolysaccharide-induced acute lung injury (ALI).BMC pharmacology & toxicology · 2024Article
- The therapeutic potential ofHeliyon · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeVentilator-induced lung injury (VILI) is a serious complication of mechanical ventilation (MV) that increases morbidity and mortality of patients receiving ventilator treatment. This study aimed to reveal the molecular mechanism of sodium houttuyfonate (SH) on VILI. MATERIALS AND
methodsThe male mice VILI model was established by high tidal volume ventilation. The cell model was established by performing cell stretch (CS) experiments on murine respiratory epithelial cells MLE-15. In addition, the JNK activator Anisomycin and JNK inhibitor SP600125 were used on VILI mice and CS-treated cells.
resultsVILI modeling damaged the structural integrity, increased apoptosis and wet-to-dry (W/D) ratio, enhanced the levels of inflammatory factors, reactive oxygen species (ROS) and malonaldehyde (MDA), and activated JNK pathway in lung tissues. SH gavage alleviated lung injury, decreased apoptosis and W/D ratio, and reduced levels of inflammatory factors, ROS and MDA, and p-JNK/JNK expression of lung tissues in VILI mice. However, activation of JNK wiped the protective effect of SH on VILI. Contrary results were found in experiments with JNK inhibitor SP600125.
conclusionSH relieved VILI by inhibiting the ROS-mediated JNK pathway.
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Registered trials
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