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Endostar Injection Inhibits Rabbit Ear Hypertrophic Scar Formation

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This study aims to investigate the effect of Endostar injection on the rabbit ear hypertrophic scar formation and expand the use of Endostar. The rabbit ear hypertrophic scar models were established 4 weeks postoperation and were treated with Endostar injection; the control group was injected with saline, once a week, 3 times totally. At the seventh week, the scar tissue was harvested and processed with hematoxylin and eosin (HE) staining and CD34 immunohistochemistry and cell apoptosis assay. In addition, the endothelial cell was cultured and seeded on Martrigel with different concentrations of Endostar to observe the vessel tube formation. The results showed that the volume of the hypertrophic scar with Endostar injection was greatly reduced compared with what was seen in the control group; meanwhile, HE staining showed that the cell number decreased and collagen density became looser. In addition, the CD34 staining indicated that microvessel formation in the study group also decreased and cell apoptosis increased. In vitro, the addition of Endostar could reduce vessel tube formation in a dose-dependent manner. In conclusion, the Endostar is effective for hypertrophic scar inhibition and could be a potential tool to treat scars.
Title: Endostar Injection Inhibits Rabbit Ear Hypertrophic Scar Formation
Description:
This study aims to investigate the effect of Endostar injection on the rabbit ear hypertrophic scar formation and expand the use of Endostar.
The rabbit ear hypertrophic scar models were established 4 weeks postoperation and were treated with Endostar injection; the control group was injected with saline, once a week, 3 times totally.
At the seventh week, the scar tissue was harvested and processed with hematoxylin and eosin (HE) staining and CD34 immunohistochemistry and cell apoptosis assay.
In addition, the endothelial cell was cultured and seeded on Martrigel with different concentrations of Endostar to observe the vessel tube formation.
The results showed that the volume of the hypertrophic scar with Endostar injection was greatly reduced compared with what was seen in the control group; meanwhile, HE staining showed that the cell number decreased and collagen density became looser.
In addition, the CD34 staining indicated that microvessel formation in the study group also decreased and cell apoptosis increased.
In vitro, the addition of Endostar could reduce vessel tube formation in a dose-dependent manner.
In conclusion, the Endostar is effective for hypertrophic scar inhibition and could be a potential tool to treat scars.

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