ArticleOxidative medicine and cellular longevity2022
Salvianolic Acid A Protects against Lipopolysaccharide-Induced Acute Lung Injury by Inhibiting Neutrophil NETosis.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Qingwen Baidu Decoction attenuates acute lung injury via macrophage exosomal miR-146a suppression of alveolar epithelial cell pyroptosis.Journal of traditional and complementary medicine · 2026Article
- Salvianolic Acid A Relieves Acute Lung Injury by Promoting the Expression of FOXO1 and Activating Autophagy Through the Inhibition of miR-217-5p.Biochemical genetics · 2026Article
- Salvianolic acid A reduces lipotoxicity injury of cardiomyocytes by orchestrating oxidative stress and inflammation via Akt/Nrf2/NF-κB axis.Journal of molecular histology · 2025Article
- A novel anti-acute lung injury mechanism of astilbin: inhibition of epithelial cells ferroptosis by targeting NRF2 activation via binding Val608 site of NRF2.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Advances in acute respiratory distress syndrome: focusing on heterogeneity, pathophysiology, and therapeutic strategies.Signal transduction and targeted therapy · 2025Review
- Neutrophil extracellular traps in homeostasis and disease.Signal transduction and targeted therapy · 2024Review
- Research Progress on Regulation of Immune Response by Tanshinones and Salvianolic Acids of Danshen (Molecules (Basel, Switzerland) · 2024Review
- Qingfei Huoxue Decoction and Its Active Component Narirutin Alleviate LPS-Induced Acute Lung Injury by Regulating TLR4/NF-κB Pathway Mediated Inflammation.Journal of inflammation research · 2024Article
- Neutrophil-specific ORAI1 Calcium Channel Inhibition Reduces Pancreatitis-associated Acute Lung Injury.Function (Oxford, England) · 2024Article
- Phenolic acids from medicinal and edible homologous plants: a potential anti-inflammatory agent for inflammatory diseases.Frontiers in immunology · 2024Review
- Reactive Oxygen Species and Strategies for Antioxidant Intervention in Acute Respiratory Distress Syndrome.Antioxidants (Basel, Switzerland) · 2023Review
- Article
- Bioactive fraction from Plumeria obtusa L. attenuates LPS-induced acute lung injury in mice and inflammation in RAW 264.7 macrophages: LC/QToF-MS and molecular docking.Inflammopharmacology · 2023Article
- Emerging Role of Neutrophil Extracellular Traps in Gastrointestinal Tumors: A Narrative Review.International journal of molecular sciences · 2022Review
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9 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Salvianolic acid A (SAA) is one of bioactive polyphenol extracted from a Salvia miltiorrhiza (Danshen), which was widely used to treat cardiovascular disease in traditional Chinese medicine. SAA has been reported to be protective in cardiovascular disease and ischemia injury, with anti-inflammatory and antioxidative effect, but its role in acute lung injury (ALI) is still unknown. In this study, we sought to investigate the therapeutic effects of SAA in a murine model of lipopolysaccharide- (LPS-) induced ALI. The optimal dose of SAA was determined by comparing the attenuation of lung injury score after administration of SAA at three different doses (low, 5 mg/kg; medium, 10 mg/kg; and, high 15 mg/kg). Dexamethasone (DEX) was used as a positive control for SAA. Here, we showed that the therapeutic effect of SAA (10 mg/kg) against LPS-induced pathologic injury in the lungs was comparable to DEX. SAA and DEX attenuated the increased W/D ratio and the protein level, counts of total cells and neutrophils, and cytokine levels in the BALF of ALI mice similarly. The oxidative stress was also relieved by SAA and DEX according to the superoxide dismutase and malondialdehyde. NET level in the lungs was elevated in the injured lung while SAA and DEX reduced it significantly. LPS induced phosphorylation of Src, Raf, MEK, and ERK in the lungs, which was inhibited by SAA and DEX. NET level and phosphorylation level of Src/Raf/MEK/ERK pathway in the neutrophils from acute respiratory distress syndrome (ARDS) patients were also inhibited by SAA and DEX in vitro, but the YEEI peptide reversed the protective effect of SAA completely. The inhibition of NET release by SAA was also reversed by YEEI peptide in LPS-challenged neutrophils from healthy volunteers. Our data demonstrated that SAA ameliorated ALI via attenuating inflammation, oxidative stress, and neutrophil NETosis. The mechanism of such protective effect might involve the inhibition of Src activation.
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