Renò F, Grazianetti P, Cannas M
Laboratorio di Anatomia Umana, Dipartimento di Scienze Mediche, Università del Piemonte Orientale 'A. Avogadro', Via Solaroli 17, 28100, Novara, Italy.
Burns. 2001 May;27(3):215-8. doi: 10.1016/s0305-4179(00)00101-7.
An alteration in the normal process of tissue repair can lead to the formation of hypertrophic scars. The best prevention and control of hypertrophy, especially in burn scars, is achieved using elastocompression, through a mechanism not yet clarified. Various studies have shown that mechanical compression induces the release of prostaglandin E2 (PGE2) and that PGE2 increases the expression of collagenases. In this study, we evaluated the effect of mechanical compression in vitro on PGE2 release in human normotrophic (NS) and hypertrophic (HS) burn scars. PGE2 basal levels in HS were significantly lower than those present in NS, and compression induced a significant increase in the release of PGE2 in HS scar in remission (7.2 times basal level) and active stages (5.88 times basal level). This increase seemed to be only partially IL-1beta-dependent. These data suggest a role for PGE2 in the process of hypertrophy remission induced by pressure therapy.
组织修复正常过程的改变可导致肥厚性瘢痕的形成。使用弹性压迫法能最好地预防和控制瘢痕增生，尤其是烧伤瘢痕，但其作用机制尚不清楚。多项研究表明，机械压迫可诱导前列腺素E2（PGE2）释放，且PGE2可增加胶原酶的表达。在本研究中，我们评估了体外机械压迫对人正常营养性（NS）和肥厚性（HS）烧伤瘢痕中PGE2释放的影响。HS中PGE2的基础水平显著低于NS中的水平，压迫导致缓解期HS瘢痕（基础水平的7.2倍）和活动期HS瘢痕（基础水平的5.88倍）中PGE2的释放显著增加。这种增加似乎仅部分依赖白细胞介素-1β。这些数据表明PGE2在压力疗法诱导的增生缓解过程中发挥作用。
