Abstract
Recombinant human endostatin (Endostar) has been widely used to suppress angiogenesis in carcinoma patients. Hypertrophic scar (HS) tissue, much like a carcinoma, is often associated with angiogenesis. However, there have been few studies conducted on the effects of Endostar on HS or its mechanism. This paper investigated the effects Endostar on the HS of rabbit ears and studied the effects of Endostar on VEGF and TIMP-1 expression. Sixteen New Zealand white rabbits were used to establish HS models. Then, rabbit ears containing HS were randomly assigned to either the Endostar group or the control group. The changes of appearance and histology were evaluated using the naked eye, hematoxylin eosin staining, and a scar elevation index. The VEGF and TIMP-1 expressions were detected by immunohistochemical staining, RT-PCR, and western blot. The thickness of the connective tissue in the Endostar group were thinner, the numbers of micro vessels and fibroblasts were fewer, and the collagen fibers were smoother. Moreover, the mRNA and protein expressions of VEGF and TIMP-1 in the Endostar group were significantly lower than those in the control group. The results suggested that Endostar reduced the formation of HS by down-regulation of VEGF and TIMP-1 expressions.
Highlights
A hypertrophic scar (HS), an excessive healing reaction to injury, is characterized by excessive fibrosis and collagen deposition in extracellular matrix (ECM)[1]
Because Hypertrophic scar (HS) is associated with the occurrence of angiogenesis and Endostar is an angiogenesis inhibitor, this study aimed to investigate the effects of Endostar on HS tissue in model of rabbit ears and the effects of Endostar on Vascular endothelial growth factor (VEGF) and tissue inhibitors of metalloproteinases (TIMPs)-1 expressions
Positive staining of TIMP-1 in Endostar group (SAB×400). These results showed that the protein expressions of VEGF and TIMP-1 were significantly down-regulated by Endostar (Table 1)
Summary
A hypertrophic scar (HS), an excessive healing reaction to injury, is characterized by excessive fibrosis and collagen deposition in extracellular matrix (ECM)[1]. Endostar is a modified human endostatin with a nine amino acid sequence at the N-terminus (MGGSHHHHH) It is widely used in suppressing angiogenesis in carcinomaand is far more efficient than previous endostatins[7]. Hypertrophic scar (HS) tissue, much like a carcinoma, is often associated with angiogenesis. Objective: This paper investigated the effects Endostar on the HS of rabbit ears and studied the effects of Endostar on VEGF and TIMP-1 expression. Conclusion: The results suggested that Endostar reduced the formation of HS by down-regulation of VEGF and TIMP-1 expressions. Recombinant human endostatin reduces hypertrophic scar formation in rabbit ear model through down- regulation of VEGF and TIMP-1.
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