ArticleOxidative medicine and cellular longevity2017
Seabuckthorn Paste Protects Lipopolysaccharide-Induced Acute Lung Injury in Mice through Attenuation of Oxidative Stress.
Article in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 22 citations in OpenAlex.
- [Protective effect of dexmedetomidine against perioperative inflammation and on pulmonary function in patients undergoing radical resection of lung cancer].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017Trial
- Ergosterol alleviates lipopolysaccharide-induced acute kidney injury in rats via a mechanistic modulation of TLR4/p-p38/NF-κB, iNOS/NO and Nrf2/HO-1 signaling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The role of sea buckthorn in skin and mucosal health: a review from an anti-inflammatory perspective.Frontiers in pharmacology · 2025Review
- Protective Effects ofInternational journal of molecular sciences · 2022Article
- Aqueous extract of Whitmania pigra Whitman ameliorates ferric chloride-induced venous thrombosis in rats via antioxidation.Journal of thrombosis and thrombolysis · 2021Article
- GPA Peptide Attenuates Sepsis-Induced Acute Lung Injury in Mice via Inhibiting Oxidative Stress and Pyroptosis of Alveolar Macrophage.Oxidative medicine and cellular longevity · 2021Article
- Protection of ripasudil, a Rho kinase inhibitor, in lipopolysaccharides-induced acute pneumonia in mice.American journal of translational research · 2019Article
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
Oxidative stress is one of the major mechanisms implicated in endotoxin-induced acute lung injury. Seabuckthorn paste (SP), a traditional Tibetan medicine with high content of polyphenols and remarkable antioxidant activity, is commonly used in treating pulmonary diseases. In the present study, the protective effects and possible underlying mechanisms of SP on lipopolysaccharide- (LPS-) induced acute lung injury in mice were investigated. It was found that body weight loss, lung tissue microstructure lesions, transvascular leakage increase, malondialdehyde augmentation, and the reduction of superoxide dismutase and glutathione peroxidase levels caused by LPS challenge were all consistently relieved by SP treatment in a dose-dependent manner. Moreover, accumulation of nuclear factor erythroid 2-related factor 2 (Nrf2) in lung nuclei caused by SP treatment was observed. Our study demonstrated that SP can provide significant protection against LPS-induced acute lung injury through maintaining redox homeostasis, and its mechanism involves Nrf2 nuclear translocation and activation.
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