Dans M J, Isseroff R
Department of Dermatology, University of California, Davis 95616.
J Invest Dermatol. 1994 Jan;102(1):118-21. doi: 10.1111/1523-1747.ep12371743.
The ability to control wound contraction is important in preventing disfiguring scarring in burn and trauma patients. Fibroblasts within the wound generate the mechanical forces that cause this contraction, and their interactions with various extracellular matrix components are thought to regulate this process. Because pentoxifylline and the interferons are believed to moderate fibroblast production of such matrix components, we assessed the effects of these agents on wound contraction in vitro, using a model wherein dermal fibroblasts are incorporated into a collagen lattice. Pentoxifylline and interferon-alpha, -beta, and -gamma inhibited lattice contraction in a dose-dependent manner and showed no effect on cell number or cell viability. These results suggest that pentoxifylline and the interferons may retard wound contraction in vivo and thus reduce scarring associated with severely contracted wounds. Further study is needed to determine the mechanism of action of these agents on the collagen lattice model.
控制伤口收缩的能力对于预防烧伤和创伤患者出现毁容性瘢痕至关重要。伤口内的成纤维细胞产生导致这种收缩的机械力，并且它们与各种细胞外基质成分的相互作用被认为可调节这一过程。由于己酮可可碱和干扰素被认为可调节成纤维细胞对此类基质成分的产生，我们使用一种将真皮成纤维细胞掺入胶原晶格的模型，在体外评估了这些药物对伤口收缩的影响。己酮可可碱以及干扰素α、β和γ以剂量依赖的方式抑制晶格收缩，并且对细胞数量或细胞活力没有影响。这些结果表明，己酮可可碱和干扰素可能会在体内延缓伤口收缩，从而减少与严重收缩伤口相关的瘢痕形成。需要进一步研究以确定这些药物对胶原晶格模型的作用机制。
