Influence of anti- angiogenesis therapy on proliferation and apoptosis of fibroblasts derived from keloid
10.3760/cma.j.issn.1673-4203.2011.07.010
- VernacularTitle:抗血管生成对瘢痕疙瘩成纤维细胞增生和凋亡的影响
- Author:
Yunchun MAO
;
Xuemei MA
;
Shufang SHI
;
Yinguang GAO
;
Hongjiao QI
;
Shuyuan CHEN
- Publication Type:Journal Article
- Keywords:
Keloid;
Proliferation;
Apoptosis
- From:
International Journal of Surgery
2011;38(7):461-465,506
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the influence of anti-angiogenesis therapy on proliferation and apoptosis of fibroblasts derived from keloids. Methods Thirty pieces of keloids from a patient were implanted into subcutaneous tissue of the nude mice, 24 pieces of which survived were divided into three groups which were treated with perilesional injection of vascular endothelial growth factor( VEGF) (0.4 mg/0.2 mL) , Endostar(0.125 g/0.2 mL) and physiological saline (0.2 mL)on the 21 d, 23 d, 25 d, 27 d after implantation. Sample were collected on the 10th day after perilesional injection, the proliferating fibroblasts in keloid tissue were immunohistochemically detected by proliferating cell nuclear antigen (PCNA) expression. The apoptotic cell was detected by terminal deoxynucleotidyl transferase dUTP-nick end labeling (TUNEL) staining. Results IHC staining indicated that PCNA expression of fibroblasts was significantly increased in keloid tissue after VEGF injection, PCNA expression of fibroblasts was significantly reduced in keloid tissue after Endostar injection,TUNEL assay revealed lower apoptotic cells expression in the keloid tissue after VEGF injection and higher in the Endostar group than control group. The rate of proliferative index (PI) , apoptotic index(AI) and AI/PI of fibroblasts in keloid after VEGF (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-angiogenesis therapy is shown to induce keloid regression through suppression of keloid fibroblast proliferation,induction of apoptosis, which may be a new approach for the treatment of keloids.
