ArticleExperimental and therapeutic medicine2023
Isorhamnetin attenuates the proliferation, invasion, migration and fibrosis of keloid fibroblasts by targeting S1PR1.
Article in Experimental and therapeutic medicine, 2023. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Insights into How Plant-Derived Extracts and Compounds Can Help in the Prevention and Treatment of Keloid Disease: Established and Emerging Therapeutic Targets.International journal of molecular sciences · 2024Review
- RadixJournal of inflammation research · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Isorhamnetin (IH) is a type of flavonoid with multiple biological activities, including cardioprotective, antitumor, anti-inflammatory and antioxidant activities. However, the role and potential mechanism of IH in keloids are still not completely understood. The aim of the present study was to explore how IH affects keloid progression. In the present study, cell proliferation was evaluated using the Cell Counting Kit-8 assay and immunofluorescence. Wound healing and Transwell assays were performed to assess cell migration and invasion, respectively. The expression levels of fibrosis-related proteins were measured using western blot analysis and immunofluorescence. In addition, the binding between IH and sphingosine-1-phosphate receptor-1 (S1PR1) was analyzed using the TargetNet database, and molecular docking was performed using Zinc, PubChem, AutoDockTools 1.5.6 and Discovery Studio 4.5 software. The expression levels of proteins in the PI3K/AKT pathway were detected by western blot analysis. The results showed that IH inhibited the proliferation, invasion, migration and fibrosis of keloid fibroblasts. The binding of IH and S1PR1 was verified and molecular docking was performed. Notably, IH significantly suppressed the expression levels of S1PR1, phosphorylated (p)-PI3K and p-AKT. Furthermore, the silencing of S1PR1 suppressed the cell proliferation, migration, invasion and fibrosis of keloid fibroblasts, as well as the expression of the PI3K/AKT pathway proteins. Conversely, S1PR1 upregulation reversed the inhibitory effects of IH on keloid fibroblast proliferation, migration, invasion and fibrosis. In conclusion, the results revealed that IH suppressed the proliferation, migration, invasion and fibrosis of keloid fibroblasts by targeting the S1PR1/PI3K/AKT pathway, suggesting that IH may be a promising drug for the treatment of keloids.
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