Androstenediol reverses steroid-inhibited wound healing.
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.
Feeser
V Ramana
VR
Department of Emergency Medicine, Reanimation, Engineering and Shock Center, VCU Medical Center, Virginia Commonwealth University, 1101 East Marshall Street, Richmond, VA 23298, USA.
Menke
Nathan B
NB
Ward
Kevin R
KR
Loria
Roger M
RM
Diegelmann
Robert F
RF
D045930:Anabolic Agents / Q000494:pharmacology*; D015114:Androstenediol / Q000494:pharmacology*; D000818:Animals; D004195:Disease Models, Animal; D005938:Glucocorticoids / Q000494:pharmacology*; D008297:Male; D008775:Methylprednisolone / Q000494:pharmacology*; D051379:Mice; D012867:Skin / Q000187:drug effects / Q000293:injuries; D014945:Wound Healing / Q000187:drug effects* / Q000276:immunology; D014947:Wounds and Injuries / Q000188:drug therapy* / Q000276:immunology
D045930:Anabolic Agents; D005938:Glucocorticoids; D015114:Androstenediol; D008775:Methylprednisolone