Cohen I K, Diegelmann R F, Johnson M L
Surgery. 1977 Jul;82(1):15-20.
Contraction and epithelization are two phenomena of "wound healing" retarded by corticosteroids. It is unclear how these agents affect collagen synthesis and wound remodeling. The methods used by several authors to conclude that steroids inhibit collagen synthesis are questioned. Therefore, collagen synthesis was measured in cultured steroid-treated chick embryo calvaria, 5 day open wounds in treated rats, and intralesionally injected human keloids. Collagen synthesis was suppressed only by long-term administration of massive systemic doses of a sustained release form of methylprednisolone (Depo-Medrol). Large, intermittent doses of corticosteroids (triamcinolone and Solu-Medrol) did not alter collagen synthesis. Because human keloids become softer and smaller following intralesional administration of triamcinolone without lowering the normally high rate of collagen synthesis, we hypothesize that corticosteroids enhance collagen degradation.
收缩和上皮形成是“伤口愈合”过程中受皮质类固醇抑制的两种现象。目前尚不清楚这些药物如何影响胶原蛋白合成和伤口重塑。几位作者用于得出类固醇抑制胶原蛋白合成结论的方法受到质疑。因此,我们在培养的经类固醇处理的鸡胚颅骨、经处理大鼠的5天开放性伤口以及病灶内注射的人瘢痕疙瘩中测量了胶原蛋白合成。仅长期大剂量全身给予持续释放形式的甲泼尼龙(德宝松)会抑制胶原蛋白合成。大剂量间歇性给予皮质类固醇(曲安奈德和甲强龙)不会改变胶原蛋白合成。由于在病灶内注射曲安奈德后人瘢痕疙瘩会变软变小,而不会降低原本就很高的胶原蛋白合成速率,我们推测皮质类固醇会增强胶原蛋白降解。