ArticleCell biochemistry and biophysics2022
Taraxasterol Inhibits Hyperactivation of Macrophages to Alleviate the Sepsis-induced Inflammatory Response of ARDS Rats.
Article in Cell biochemistry and biophysics, 2022. 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, 7 citations in OpenAlex.
- Structure-activity relationships and molecular mechanisms of natural products in sepsis-associated organ dysfunction: a narrative review.Frontiers in pharmacology · 2026Review
- Taraxasterol attenuates inflammatory responses in a 2,4-dinitrochlorobenzene-induced atopic dermatitis mouse model via inactivation of the MAPK and NF-κB pathways.Journal of molecular histology · 2025Article
- Macrophage‑driven pathogenesis in acute lung injury/acute respiratory disease syndrome: Harnessing natural products for therapeutic interventions (Review).Molecular medicine reports · 2025Review
- Experimental animal models of acute respiratory distress syndrome: one-hit and two-hit establishment application.Frontiers in immunology · 2025Review
- A comparative analysis of sivelestat sodium hydrate and ulinastatin combination therapy in the treatment of sepsis with acute respiratory distress syndrome.BMC pulmonary medicine · 2024Article
- Pharmacological Action and Research Progress of Taraxasterol.Current pharmaceutical biotechnology · 2024Review
- Fusu mixture alleviates inflammatory reactions in lipopolysaccharide-induced acute respiratory distress syndrome mice via regulation of surfactant-associated protein C, aquaporin 5, and Notch1.Journal of thoracic disease · 2023Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To explore the effect and mechanism of taraxasterol on sepsis-induced acute respiratory distress syndrome (ARDS). Twenty-four male SD rats were randomly divided into four groups: the control group, model (lipopolysaccharide, LPS) group, lipopolysaccharide+taraxasterol (LPS + TXL) group, and lipopolysaccharide+ulinastatin (LPS + UTI) group. The model of sepsis-induced ARDS was established by intraperitoneal injection of LPS. The lung water content of the rats in each group was determined by the dry/wet ratio. Pathology of rat lung tissue was observed through H&E staining. Wright staining was applied to count the number of neutrophils, macrophages, and total cells. ELISA was utilized to measure the levels of the inflammatory factors TNF-α, IL-1β, and IL-6 in bronchoalveolar lavage fluid (BALF). Biochemical detection was adopted to check the levels of myeloperoxidase (MPO), superoxide dismutase (SOD) and catalase (CAT) in lung tissue. Western blotting was performed to check the protein expression of IL-12, iNOS, Arg-1, and Mrc1 in lung tissue. Compared with the LPS group, both taraxasterol and ulinastatin significantly decreased lung tissue water content, improved lung tissue injury, reduced the number of neutrophils, macrophages and total cells, and decreased the level of inflammatory factors. In addition, taraxasterol and ulinastatin also reduced the content of MPO and the expression of IL-12 and iNOS and increased the activity of SOD and CAT as well as the protein expression of Arg-1 and Mrc1. Taraxasterol can suppress macrophage M1 polarization to alleviate the inflammatory response and oxidative stress, thereby treating sepsis-induced ARDS.
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