Ammann A J, Beck L S, DeGuzman L, Hirabayashi S E, Lee W P, McFatridge L, Nguyen T, Xu Y, Mustoe T A
Genentech, Inc., South San Francisco, California.
Ann N Y Acad Sci. 1990;593:124-34. doi: 10.1111/j.1749-6632.1990.tb16105.x.
Previous studies have demonstrated that TGF-beta possesses many of the biologic properties necessary for acceleration of the normal wound healing process. We report that recombinant human TGF-beta 2 (rhuTGF-beta 1) increases wound strength and accelerates wound closure when applied topically to experimental wounds. Doses of 5 to 1,000 ng/wound increased wound strength in a dose-response manner and wound strength increase as high as 161% above control in the rat incisional wound model. Increased wound strength was observed as early as 3 days following rhuTGF-beta 1 application and continued to Day 28. In the rabbit ear ulcer model, acceleration of wound closure was observed following doses of 5 to 100 ng/wound applied a single topical application. No adverse effects of rhuTGF-beta 1 were observed. The amount of fibrous tissue, scar formation, and mitotic figures were not significantly greater than control. Epithelialization of rhuTGF-beta 1-treated wounds was not impeded. rhuTGF-beta 1 induced bone formation in the rabbit ear ulcer model but not in the rat incisional model, suggesting that precursor cells, such as perichondrial cells, are required for the bone forming activities of TGF-beta 1.
先前的研究表明，转化生长因子-β（TGF-β）具有加速正常伤口愈合过程所需的许多生物学特性。我们报告，当将重组人转化生长因子-β2（rhuTGF-β1）局部应用于实验性伤口时，可增加伤口强度并加速伤口闭合。在大鼠切口伤口模型中，每伤口5至1000纳克的剂量以剂量反应方式增加伤口强度，伤口强度增加高达对照的161%。在应用rhuTGF-β1后最早3天就观察到伤口强度增加，并持续到第28天。在兔耳溃疡模型中，单次局部应用每伤口5至100纳克的剂量后观察到伤口闭合加速。未观察到rhuTGF-β1的不良反应。纤维组织量、瘢痕形成和有丝分裂图均不显著大于对照。rhuTGF-β1处理的伤口的上皮形成未受阻碍。rhuTGF-β1在兔耳溃疡模型中诱导骨形成，但在大鼠切口模型中未诱导，这表明转化生长因子-β1的骨形成活性需要前体细胞，如软骨膜细胞。
