ArticleRegenerative biomaterials2024
Corilagin functionalized decellularized extracellular matrix as artificial blood vessels with improved endothelialization and anti-inflammation by reactive oxygen species scavenging.
Article in Regenerative biomaterials, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Preparation and evaluation of a small-diameter vascular graft with dual anticoagulant and anticalcification functions.Regenerative biomaterials · 2026Article
- Biomimetic lung-targeting vehicle coupled with cryo-shocked leukocyte and inflammation-anchored liposome for drug delivery and anti-inflammation in treatment of acute pneumonia.Regenerative biomaterials · 2026Article
- [Research progress on calcification mechanism and anti-calcification strategies of vascular grafts].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2025Review
- Green Approach forAntioxidants (Basel, Switzerland) · 2025Article
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Authors and funding
13 authors.
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Abstract
The performance of biological-originated blood vessels in clinical remains disappointing due to fast occlusion caused by acute thrombosis or long-standing inflammation. How to prevent rapid degradation and inhibit acute inflammation but maintain their high bioactivity is still a significant challenge. As a bioactive polyphenol in various traditional Chinese medicine, Corilagin (Cor) exhibits excellent anticoagulant, anti-inflammatory and rapid ROS consumption properties. Inspired by abundant supramolecular interactions in organisms, we selected it to crosslink tissues via purely H-bonds to simulate these natural interactions without introducing potential toxic aldehyde or carboxyl groups. Results show that 2 mg/ml was selected as the optimal Cor concentration to form a stable crosslinking network (FI > 95%) and effectively delay their degradation. Cor modification not only enhances ECs adhesion and monolayer function via accelerating VEGF and TGF-β secretion but also promotes macrophage transformation from pro-inflammatory M1 phenotype to anti-inflammatory M2 ones.
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