Feeser V Ramana, Menke Nathan B, Ward Kevin R, Loria Roger M, Diegelmann Robert F
Department of Emergency Medicine, Reanimation, Engineering and Shock Center, VCU Medical Center, Virginia Commonwealth University, 1101 East Marshall Street, Richmond, VA 23298, USA.
Wound Repair Regen. 2009 Sep-Oct;17(5):758-61. doi: 10.1111/j.1524-475X.2009.00528.x.
It is well recognized that stress of any nature will cause a delay in the wound healing response. This delayed healing response appears closely associated with immune regulators. In this study, CD-1 mice were injected with a long acting form of methyl prednisolone to cause a steroid-induced immune suppression. After 24 hours, two 6-mm full thickness wounds were placed on the animals' backs and one group of animals received the immune-regulating hormone, androstenediol. Wound contraction was quantified by planimetry for the subsequent 14 days. Animals that were stressed with methyl prednisolone but receiving androstenediol contracted their open wounds at faster rates compared with methyl prednisolone-stressed animals treated with the vehicle alone. These findings suggest that restoration of immune regulation by androstenediol can reverse the delayed open wound contraction secondary to steroid stress.
人们已经充分认识到，任何性质的应激都会导致伤口愈合反应延迟。这种延迟的愈合反应似乎与免疫调节因子密切相关。在本研究中，给CD-1小鼠注射长效甲基强的松龙以引起类固醇诱导的免疫抑制。24小时后，在动物背部制造两个6毫米的全层伤口，一组动物接受免疫调节激素雄烯二醇。在随后的14天内通过平面测量法对伤口收缩进行量化。与仅接受赋形剂治疗的甲基强的松龙应激动物相比，接受甲基强的松龙应激但同时接受雄烯二醇的动物以更快的速度收缩其开放性伤口。这些发现表明，雄烯二醇恢复免疫调节可以逆转类固醇应激继发的开放性伤口收缩延迟。
