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- Title
Effect of atorvastatin on lipopolysaccharide-induced lung inflammation and hypoxia in mice; modulation of HIF-1α, CINC and MIP-2.
- Authors
Salama, Abeer; El-Fadaly, Amany A.; Elgohary, Rania
- Abstract
Background: Acute lung injury is a crucial pathological state, particularly in some severe infectious respiratory illnesses, distinguished by acute inflammation, pulmonary edema, hypoxia, and neutrophil recruitment. Cytokine-induced neutrophil chemoattractant (CINC) and macrophage inflammatory protein-2 (MIP-2) play a vital role in neutrophil recruitment. Objective: Here, we validated the potential repressing effect of atorvastatin on acute lung injury induced by lipopolysaccharide (LPS) in mice. Materials and methods: Mice were injected with LPS (250 μg/kg; i.p.) daily for 7 days, and atorvastatin (25 and 50 mg/kg; orally) daily along with LPS. Results: Atorvastatin ameliorated oxidative stress as evidenced by increased reduced glutathione (GSH) and nuclear factor-erythroid 2 related factor 2 (Nrf2) levels and decreased malondialdehyde (MDA) levels. Additionally, it lessened inflammatory biomarkers including tumor necrosis factor-alpha (TNF-α), mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), CINC, and MIP-2, as well as hypoxia biomarker hypoxia-inducible factor–1α (HIF-1α). Moreover, atorvastatin slowed the progression of lung tissue histological lesions. Conclusion: Collectively, the present study suggests that, atorvastatin effectively protects against LPS-induced acute lung injury through inhibition of oxidative stress, inflammation, hypoxia, and neutrophil recruitment.
- Subjects
MACROPHAGE inflammatory proteins; TUMOR necrosis factors; MITOGEN-activated protein kinases; PULMONARY edema; PNEUMONIA
- Publication
Immunopharmacology & Immunotoxicology, 2025, Vol 47, Issue 1, p85
- ISSN
0892-3973
- Publication type
Academic Journal
- DOI
10.1080/08923973.2024.2436089