RESUMO
Excessive blood loss could lead to pathological conditions such as tissue necrosis, organ failure, and death. The limitations of recently developed hemostatic approaches, such as their low mechanical strength, inadequate wet tissue adhesion, and weak hemostatic activity, pose challenges for their application in controlling visceral bleeding. In this study, a novel hydrogel (CT) made of collagen and tannic acid (TA) was proposed. By altering the proportions between the two materials, the mechanical properties, adhesion, and coagulation ability were evaluated. Compared to commercial hydrogels, this hydrogel has shown reduced blood loss and shorter hemostatic time in rat hepatic and cardiac bleeding models. This was explained by the hydrogel's natural hemostatic properties and the significant benefits of wound closure in a moist environment. Better biodegradability was achieved through the non-covalent connection between tannic acid and collagen, allowing for hemostasis without hindering subsequent tissue repair. Therefore, this hydrogel is a new method for visceral hemostasis that offers significant advantages in treating acute wounds and controlling major bleeding. And the production method is simple and efficient, which facilitates its translation to clinical applications.
RESUMO
The effect and mechanism of type III recombinant humanized collagen (hCOLIII) on human vascular endothelial EA.hy926 cells at the cellular and molecular levels were investigated. The impact of hCOLIII on the proliferation of EA.hy926 cells was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromid assay, the effect of hCOLIII on cell migration was investigated by scratch assay, the impact of hCOLIII on cell cycle and apoptosis was detected by flow cytometry, the ability of hCOLIII to induce angiogenesis of EA.hy926 cells was evaluated by angiogenesis assay, and the effect of hCOLIII on vascular endothelial growth factor (VEGF) expression was detected by real-time reverse transcription-polymerase chain reaction analysis. The hCOLIII at concentrations of 0.5, 0.25, and 0.125 mg/mL all showed specific effects on the proliferation and migration of human vascular endothelial cells. It could also affect the cell cycle, increase the proliferation index, and increase the expression level of VEGF in human vascular endothelial cells. In the meantime, hCOLIII at the concentration of 0.5 mg/mL also showed a promoting effect on vessel formation. hCOLIII can potentially promote the endothelization process of blood vessels, mainly by affecting the proliferation, migration, and vascular-like structure of human endothelial cells. At the same time, hCOLIII can promote the expression of VEGF. This collagen demonstrated its potential as a raw material for cardiovascular implants.