The role of oxidised regenerated cellulose/collagen in wound repair: effects in vitro on fibroblast biology and in vivo in a model of compromised healing

被引:90
作者
Hart, J
Silcock, D
Gunnigle, S
Cullen, B [1 ]
Light, ND
Watt, PW
机构
[1] Johnson & Johnson Wound Management, R&D Dept, Div ETHICON, Gargrave BD23 3RX, N Yorkshire, England
[2] Univ Leeds, St Jamess Univ Hosp, Mol Med Unit, Wound Repair Programme, Leeds LS9 7TF, W Yorkshire, England
关键词
fibroblast migration/proliferation; delayed wound healing; biomaterial; diabetes;
D O I
10.1016/S1357-2725(02)00062-6
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
Irrespective of underlying chronic wound pathology, delayed wound healing is normally characterised by impaired new tissue formation at the site of injury. It is thought that this impairment reflects both a reduced capacity to synthesize new tissue and the antagonistic activities of high levels of proteinases within the chronic wound environment. Historically, wound dressings have largely been passive devices that offer the wound interim barrier function and establish a moist healing. environment. A new generation of devices, designed to interact with the wound and promote new tissue formation, is currently being developed and tested. This study considers one such device, oxidised regenerated cellulose (ORC)/collagen, in terms of its ability to promote fibroblast migration and proliferation in vitro and to accelerate wound repair in the diabetic mouse, a model of delayed wound healing. ORC/collagen was found to promote both human dermal fibroblasts proliferation and cell migration. In vivo studies considered the closure and histological characteristics of diabetic wounds treated with ORC/collagen compared to those of wounds given standard treatment on both diabetic and non-diabetic mice. ORC/collagen was found to significantly accelerate diabetic wound closure and result in a measurable improvement in the histological appearance of wound tissues. As the diabetic mouse is a recognised model of impaired healing, which may share some characteristics of human chronic wounds, the results of this in vivo study, taken together with those relating the positive effects of ORC/collagen in vitro, may predict the beneficial use of this device in the clinical setting. (C) 2002 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:1557 / 1570
页数:14
相关论文
共 69 条
[1]
Abd-El-Aleem SA, 2000, J PATHOL, V191, P434, DOI 10.1002/1096-9896(2000)9999:9999<::AID-PATH654>3.0.CO
[2]
2-S
[3]
ALBINI A, 1985, EUR J CELL BIOL, V36, P104
[4]
The fate of collagen implants in tissue defects [J].
Bailey, AJ .
WOUND REPAIR AND REGENERATION, 2000, 8 (01) :5-12
[5]
Barone EJ, 1998, PLAST RECONSTR SURG, V102, P1023, DOI 10.1097/00006534-199809040-00015
[6]
Reduced expression of PDGF and PDGF receptors during impaired wound healing [J].
Beer, HD ;
Longaker, MT ;
Werner, S .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1997, 109 (02) :132-138
[7]
Transforming growth factor-beta and insulin-like growth factor-1 in relation to diabetes-induced impairment of wound healing [J].
Bitar, MS ;
Labbad, ZN .
JOURNAL OF SURGICAL RESEARCH, 1996, 61 (01) :113-119
[8]
PREVENTION OF TISSUE-DAMAGE - INHIBITION OF MYELOPEROXIDASE MEDIATED INACTIVATION OF ALPHA-1-PROTEINASE INHIBITOR BY N-ACETYL CYSTEINE, GLUTATHIONE, AND METHIONINE [J].
BORREGAARD, N ;
JENSEN, HS ;
BJERRUM, OW .
AGENTS AND ACTIONS, 1987, 22 (3-4) :255-260
[9]
BROWN AF, 1984, SCANNING ELECTRON MI, V2, P747
[10]
Apoptosis down-regulates inflammation under the advancing epithelial wound edge: Delayed patterns in diabetes and improvement with topical growth factors [J].
Brown, DL ;
Kao, WWY ;
Greenhalgh, DG .
SURGERY, 1997, 121 (04) :372-380