ArticleThe clinical respiratory journal2024
Linoleic Acid Promotes Mitochondrial Biogenesis and Alleviates Acute Lung Injury.
Article in The clinical respiratory journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Article
- Lactiplantibacillus plantarum GUANKE ameliorates influenza a virus-induced inflammation and lung barrier dysfunction through enhancing mitophagy and improving oxidative phosphorylation.Cellular and molecular life sciences : CMLS · 2026Article
- Macrophage Membrane-Camouflaged Mesoporous Polydopamine Nanoparticles for Targeted Delivery of Apigenin in Sepsis-Induced Acute Lung Injury.International journal of nanomedicine · 2026Article
- Comparative Phytochemical Analysis and Antimicrobial Properties of Ethanol and Macerated Extracts from Aerial and Root Parts ofMolecules (Basel, Switzerland) · 2025Article
- Dietary wet fermented Brewer's grains modulate hepatic metabolism in pullets.Scientific reports · 2025Article
- Serum metabolomics reveal the mechanisms by which fermented brewer's spent grains promote intestinal development in white-feathered broilers.Frontiers in veterinary science · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
introductionAcute lung injury (ALI) is a critical and lethal medical condition. This syndrome is characterized by an imbalance in the body's oxidation stress and inflammation. Linoleic acid (LA), a polyunsaturated fatty acid, has been extensively studied for its potential health benefits, including anti-inflammatory and antioxidant activities. However, the therapeutic effects of LA on ALI remain unexplored.
methodsLipopolysaccharide (LPS), found in gram-negative bacteria's outer membrane, was intraperitoneally injected to induce ALI in mice. In vitro model was established by LPS stimulation of mouse lung epithelial 12 (MLE-12) cells.
resultsLA treatment demonstrated a significant amelioration in LPS-induced hypothermia, poor state, and pulmonary injury in mice. LA treatment resulted in a reduction in the concentration of bronchoalveolar lavage fluid (BALF) protein and an increase in myeloperoxidase (MPO) activity in LPS-induced mice. LA treatment reduced the generation of white blood cells. LA treatment reduced cell-free (cfDNA) release and promote adenosine triphosphate (ATP) production. LA increased the levels of superoxide dismutase (SOD) and glutathione (GSH) but decreased the production of malondialdehyde (MDA). LA treatment enhanced mitochondrial membrane potential. LA attenuated LPS-induced elevations of inflammatory cytokines in both mice and cells. Additionally, LA exerted its protective effect against LPS-induced damage through activation of the peroxisome proliferator-activated receptor γ coactivator l alpha (PGC-1α)/nuclear respiratory factor 1 (NRF1)/transcription factor A of the mitochondrion (TFAM) pathway.
conclusionLA may reduce inflammation and stimulate mitochondrial biogenesis in ALI mice and MLE-12 cells.
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