ArticleInternational journal of molecular sciences2022
Amelioration of Endotoxin-Induced Acute Lung Injury and Alveolar Epithelial Cells Apoptosis by Simvastatin Is Associated with Up-Regulation of Survivin/NF-kB/p65 Pathway.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 52 citations in OpenAlex.
- Drug repurposing of sophoridine for sepsis-induced organ injury: from in-depth analysis of a single agent to a multi-target therapeutic paradigm.Frontiers in pharmacology · 2026Review
- Article
- Observational
- Effects of simvastatin pretreatment on platelet activation and hypercoagulable state in septic mice.European journal of medical research · 2025Article
- Advances in anti-inflammatory treatment of sepsis-associated acute respiratory distress syndrome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Stem cell therapy for intervertebral disc degeneration: Clinical progress with exosomes and gene vectors.World journal of stem cells · 2025Review
- Simvastatin mitigates ventilator-induced lung injury in mice with acute respiratory distress syndrome via a mechanism partly dependent on neutrophil extracellular traps.European journal of medical research · 2025Article
- CircRBM33 competitively binds miR-15a-5p to mediate EZH1 expression to ameliorate sepsis-induced acute lung injury.Clinics (Sao Paulo, Brazil) · 2025Article
- Alveolar epithelial cells in bacterial sepsis-associated acute lung injury: mechanisms and therapeutic strategies.Frontiers in immunology · 2025Review
- Atorvastatin Alleviates Sepsis-Induced Cardiomyopathy by Targeting the METTL3/IGF2BP1/CXCL2 Pathway.Journal of inflammation research · 2025Article
- Liraglutide Protects Cardiomyocytes against Isoprenaline-Induced Apoptosis in Experimental Takotsubo Syndrome.Biomedicines · 2024Article
- Saponins fromMolecules (Basel, Switzerland) · 2024Article
- TRAF4 regulates ubiquitination-modulated survivin turnover and confers radioresistance.International journal of biological sciences · 2024Article
- OAS3 Deubiquitination Due to E3 Ligase TRIM21 Downregulation Promotes Epithelial Cell Apoptosis and Drives Sepsis-induced Acute Lung Injury.International journal of biological sciences · 2024Article
- Interleukin-36 is overexpressed in human sepsis and IL-36 receptor deletion aggravates lung injury and mortality through epithelial cells and fibroblasts in experimental murine sepsis.Critical care (London, England) · 2023Article
- Research Progress and Molecular Mechanisms of Endothelial Cells Inflammation in Vascular-Related Diseases.Journal of inflammation research · 2023Review
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disruption of the alveolar−endothelial barrier caused by inflammation leads to the progression of septic acute lung injury (ALI). In the present study, we investigated the beneficial effects of simvastatin on the endotoxin lipopolysaccharide (LPS)-induced ALI and its related mechanisms. A model of ALI was induced within experimental sepsis developed by intraperitoneal injection of a single non-lethal LPS dose after short-term simvastatin pretreatment (10−40 mg/kg orally). The severity of the lung tissue inflammatory injury was expressed as pulmonary damage scores (PDS). Alveolar epithelial cell apoptosis was confirmed by TUNEL assay (DNA fragmentation) and expressed as an apoptotic index (AI), and immunohistochemically for cleaved caspase-3, cytochrome C, and anti-apoptotic Bcl-xL, an inhibitor of apoptosis, survivin, and transcriptional factor, NF-kB/p65. Severe inflammatory injury of pulmonary parenchyma (PDS 3.33 ± 0.48) was developed after the LPS challenge, whereas simvastatin significantly and dose-dependently protected lung histology after LPS (p < 0.01). Simvastatin in a dose of 40 mg/kg showed the most significant effects in amelioration alveolar epithelial cells apoptosis, demonstrating this as a marked decrease of AI (p < 0.01 vs. LPS), cytochrome C, and cleaved caspase-3 expression. Furthermore, simvastatin significantly enhanced the expression of Bcl-xL and survivin. Finally, the expression of survivin and its regulator NF-kB/p65 in the alveolar epithelium was in strong positive correlation across the groups. Simvastatin could play a protective role against LPS-induced ALI and apoptosis of the alveolar−endothelial barrier. Taken together, these effects were seemingly mediated by inhibition of caspase 3 and cytochrome C, a finding that might be associated with the up-regulation of cell-survival survivin/NF-kB/p65 pathway and Bcl-xL.
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