Comparison of the burn wound and diabetic ulcer wound.
- Author:
Cai LIN
1
;
Liang QIAO
;
Peng ZHANG
;
Geng-xin CHEN
;
Jian-jun XU
;
Ning YANG
;
Shu-liang LU
Author Information
- Publication Type:Journal Article
- MeSH: Burns; complications; metabolism; pathology; Cells, Cultured; Diabetic Foot; pathology; Fibroblast Growth Factor 2; metabolism; Foot Ulcer; etiology; pathology; Humans; Neovascularization, Physiologic; Vascular Endothelial Growth Factor A; metabolism; Wound Healing
- From: Chinese Journal of Burns 2007;23(5):339-341
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo compare the difference between the burn wound and diabetic ulcer wound, and to preliminarily analyze the nonhealing mechanism of diabetic unclear.
METHODSThe tissue of foot ulcer of diabete patients and skin wound tissues from burn patients were harvested. The levels of (FGF)2 and VEGF in the wound tissues were determined after tissue cultivation with enzyme-linked immunosorbent assay (ELISA). The changes in micro-vascular density (MVD) were examined by immunohistochemistry. Human umbilical vein endothelial cells were cultured in medium containing different components, and divided into following groups: A (with treatment of 5 mmol/L glucose for 7 days), B (with treatment of 30 mmol/L glucose for 7 days) and C (with treatment of 30 mmol/L Mannitol for 7 days) groups, then the level of VEGF protein was determined by ELISA.
RESULTSThe levels of FGF2 and VEGF protein in the burn wound were (59 +/- 3) ng/ml and (56 +/- 7) pg/ml, respectively, which were obviously lower than those in diabetic ulcer wound [(89 +/- 6) ng/ml, (108 +/- 5) pg/ml, P < 0.05]. There was also obvious difference in MVD between two kinds of wound (P < 0.05). The level of VEGF protein in both wounds were similar after the addition of FGF2 to the cell culture in vitro, while there were statistically significant difference 2 and 5 days after removal of FGF.
CONCLUSIONThe nonhealing mechanism of diabetic ulcer wound may be related to the inhibition of vacuolation and low expression of factors controlling vessel growth.