Influence of anti-angiogenesis therapy on proliferation and apoptosis of fibroblasts derived from keloid

Abstract

：Objective To investigatethe influence of anti-angiogenesis therapy on proliferation and apoptosis of fibroblastsderived from keloids. Methods Thirty pieces of keloids from a patient were implanted intosubcutaneous tissue of the nude mice, 24 pieces of which survived were divided into threegroups which were treated with perilesional injection of vascular endothelial growthfactor( VEGF) (0.4 mg/0.2 mL) , Endostar(0.125 g/0.2 mL) and physiological saline (0.2mL)on the 21 d, 23 d, 25 d, 27 d after implantation. Sample were collected on the 10th dayafter perilesional injection, the proliferating fibroblasts in keloid tissue wereimmunohistochemically detected by proliferating cell nuclear antigen (PCNA) expression.The apoptotic cell was detected by terminal deoxynucleotidyl transferase dUTP-nick endlabeling (TUNEL) staining. Results IHC staining indicated that PCNA expression offibroblasts was significantly increased in keloid tissue after VEGF injection, PCNAexpression of fibroblasts was significantly reduced in keloid tissue after Endostarinjection,TUNEL assay revealed lower apoptotic cells expression in the keloid tissue afterVEGF injection and higher in the Endostar group than control group. The rate ofproliferative index (PI) , apoptotic index(AI) and AI/PI of fibroblasts in keloid afterVEGF (PI:41.13 ±2.29,AI:5.75 ±1.28,AI/PI: 0.14 ± 0.04)or Endostar injection (PI:27.25±2.61,AI:11.00±1.31,AI/PI:0.41 ±0.09)and control group (PI: 34.75 ±3.62,AI:7. 88 ±1.64,AI/PI:0. 23 ±0.07) showed statistical differences. Conclusion Anti-angiogenesistherapy is shown to induce keloid regression through suppression of keloid fibroblastproliferation,induction of apoptosis, which may be a new approach for the treatment ofkeloids.