ArticleIranian journal of pharmaceutical research : IJPR
Minocycline Regulates PARP-1 and HDAC3 Pathways to Inhibit Inflammation and Oxidative Stress in LPS-Induced Acute Lung Injury.
Article in Iranian journal of pharmaceutical research : IJPR. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- A New Survey about Dual-Acting PARP/COX-2 Inhibitors as Cancer Chemopreventive Agents.Iranian journal of pharmaceutical research : IJPRReview
- Tanshinone ⅡA Inhibits Alveolar Macrophage Polarization, Inflammation and Mitochondrial Damage by Regulating the PAPR-1 Signaling Pathway.Iranian journal of pharmaceutical research : IJPRArticle
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Authors and funding
6 authors.
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Abstract
Background: Acute lung injury (ALI) is characterized by excessive lung inflammation and apoptosis of alveolar epithelial cells, resulting in acute hypoxemic respiratory failure. Minocycline, a tetracycline antibiotic, is known to have excellent anti-inflammatory activity. Objectives: The present study aims to reveal the protective effect and potential mechanism of the anti-inflammatory effects of minocycline on lipopolysaccharide (LPS)-induced ALI in mice and A549 cells. Methods: We investigated the role of minocycline in ALI mice and inflammation-induced damage to alveolar epithelial cells using various experimental approaches, including histological staining, enzyme-linked immunosorbent assay (ELISA), quantitative real-time PCR, flow cytometry, western blot analysis, and other relevant assays. Results: Pre-treatment with minocycline effectively attenuated LPS-induced ALI in vivo by inhibiting inflammation and oxidative damage, improving pathological changes in the lungs, alleviating pulmonary edema and protein exudation, and suppressing neutrophil aggregation. In vitro, minocycline suppressed the inflammatory response of human alveolar epithelial A549 cells, as evidenced by the inhibition of inflammatory cytokine and oxidative damage biomarker expression, reduction in intracellular reactive oxygen species (ROS) production, alleviation of mitochondrial damage, and inhibition of cell apoptosis. Subsequent mechanistic studies revealed that the protective effects of minocycline against ALI may be attributed to its suppression of poly (ADP-ribose) polymerase-1 (PARP-1) and histone deacetylase 3 (HDAC3) expression. Conclusions: In conclusion, our study presents minocycline as a potential candidate for ALI therapy and provides an experimental foundation for investigating its anti-inflammatory mechanisms in the treatment of ALI. Further therapeutic value awaits verification in clinical and preclinical studies.
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