The effect of hirudin modification of silk fibroin on cell growth and antithrombogenicity

- A direct thrombin inhibitor hirudin was used to modify silk fibroin.
- Antithrombogenic property of Hir-modified silk fibroin films was improved.
- Hir-modified silk fibroin films supported adhesion and proliferation of HUVECs and HAVSMCs.
- Proliferation of HAVSMCs on silk fibroin films was inhibited by increasing Hir concentration.

Thrombus formation remains a particular challenge for small-diameter vascular grafts. In this study, the direct thrombin inhibitor hirudin (Hir) was used to modify silk fibroin films in an attempt to enhance its antithrombogenic properties. Hir was successfully attached to silk fibroin and uniformly distributed in the regenerative material. Hir-modified films showed good cytocompatibility, and supported adhesion and proliferation of fibroblasts (L929), human umbilical vascular endothelial cells (HUVECs) and human aortic smooth muscle cells (HASMCs). Proliferation of HAVSMCs was inhibited by increasing Hir concentration. Activated partial thrombin time (APTT), prothrombin time (PT) and thrombin time (TT) of Hir-modified silk fibroin tubular scaffolds (SFTSs) were all increased markedly compared with fresh rabbit blood, ethanol-treated SFTS and unmodified SFTS, demonstrating the improved antithrombogenicity of SFTSs following modification with Hir.