ArticleJournal of inflammation research2021
Rosuvastatin Enhances Alveolar Fluid Clearance in Lipopolysaccharide-Induced Acute Lung Injury by Activating the Expression of Sodium Channel and Na,K-ATPase via the PI3K/AKT/Nedd4-2 Pathway.
Article in Journal of inflammation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Nanomedicine for Acute Respiratory Distress Syndrome: From Pathophysiological Mechanisms and Disease Heterogeneity to Precision Therapy.International journal of nanomedicine · 2026Review
- Alveolar Epithelial Cell Dysfunction in Acute Respiratory Distress Syndrome: Mechanistic Insights and Targeted Interventions.Biomedicines · 2025Review
- Rosuvastatin ameliorates chemically induced acute lung injury in rats by targeting ferroptosis, heat shock protein B1, and inflammation.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Exploring the Mechanism of Action of Xuebijing Injection in Treating Acute Respiratory Distress Syndrome Based on Network Pharmacology and Animal Experiments.Journal of inflammation research · 2025Article
- NaInternational journal of molecular sciences · 2024Review
- A scoring model based on clinical factors to predict postoperative moderate to severe acute respiratory distress syndrome in Stanford type A aortic dissection.BMC pulmonary medicine · 2023Article
- Long noncoding RNA signatures in intrauterine infection/inflammation-induced lung injury: an integrative bioinformatics study.BMC pulmonary medicine · 2023Article
- The Na/K-ATPase role as a signal transducer in lung inflammation.Frontiers in immunology · 2023Review
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Authors and funding
14 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are devastating clinical conditions characterized by pulmonary epithelial damage and protein-rich fluid accumulation in the alveolar spaces. Statins are a class of HMG-CoA reductase inhibitors, which exert cholesterol-lowering and anti-inflammatory effects.
methodsRosuvastatin (1 mg/kg) was injected intravenously in rats 12 h before lipopolysaccharide (LPS, 10 mg/kg) administration. Eight hours later after LPS challenge, alveolar fluid clearance (AFC) was detected in rats (n = 6-8). Rosuvastatin (0.3 µmol/mL) and LPS were cultured with primary rat alveolar type II epithelial cells for 8 h.
resultsRosuvastatin obviously improved AFC and attenuated lung-tissue damage in ALI model. Moreover, it enhanced AFC by increasing sodium channel and Na,K-ATPase protein expression. It also up-regulated P-Akt via reducing Nedd4-2 in vivo and in vitro. Furthermore, LY294002 blocked the increase in AFC in response to rosuvastatin. Rosuvastatin-induced AFC was found to be partly rely on sodium channel and Na,K-ATPase expression via the PI3K/AKT/Nedd4-2 pathway.
conclusionIn summary, the findings of our study revealed the potential role of rosuvastatin in the management of ALI/ARDS.
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