Castration and wound healing
Posted: Tue Nov 28, 2006 6:22 pm
Yet another recent study wich demonstrates the immune-improving effects of castration/androgen depletion. The authors of this particular study suggest, on the basis of their findings and several other preceding studies, that the usage of androgen receptor blockers such as Flutamide for trauma patients in order to improve the healing rate and the extent of post-surgery complications is an option worth further investigation (Actually, Richard Boyd, an Australian professor who specialize in immunobiology, is already using chemical castration as means of improving the immune function in trauma patients. See: http://www.abc.net.au/catalyst/stories/s725898.htm)
"ABSTRACT
Hypothesis: Studies indicate that a depressed wound immune function contributes to an increased rate of wound complications and impaired wound healing following trauma-hemorrhage (T-H). Androgen, ie, 5-dihydrotestosterone, is responsible for producing the depressed systemic cell-mediated immune responses following T-H in males. The aim of the present study was to determine whether depletion of 5-dihydrotestosterone in males before T-H has any salutary effects on wound immune cell function and wound healing in male mice following T-H.
Design: Mice were castrated or sham castrated 14 days before midline laparotomy (ie, tissue trauma) and subcutaneous polyvinyl sponge implantation, followed by hemorrhage (mean ± SEM blood pressure, 35 ± 5 mm Hg for 90 minutes and resuscitation) or sham operation. At 24 hours thereafter, wound immune cells from the sponges were harvested and cultured with lipopolysaccharide A. Release of interleukin 1 (IL-1) and IL-6 (in picograms per milliliter) was determined in the supernatants by enzyme-linked immunosorbent assay. In addition, IL-6 was assessed at the wound site by immunohistochemistry. Ten days after T-H, wound-breaking strength was measured.
Results: Precastration prevented the significantly suppressed capacity of wound immune cells to release IL-1 and IL-6. In addition, precastration normalized the elevated IL-6 expression at the wound site in the T-H mice. Moreover, wound-breaking strength was improved in castrated mice 10 days after T-H.
Conclusions: Male sex steroids appear to be responsible for wound immune cell dysfunction following trauma and severe blood loss. Because decreasing androgen levels resulted in improved wound healing, our results suggest that the use of androgen receptor–blocking agents, eg, flutamide, following T-H might represent a novel adjunct for decreasing the rate of wound complications under those conditions."
Complete study details and further references: http://archsurg.ama-assn.org/cgi/content/full/139/2/157
Also see: http://jcs.biologists.org/cgi/content/a ... cs.02786v1
"ABSTRACT
Hypothesis: Studies indicate that a depressed wound immune function contributes to an increased rate of wound complications and impaired wound healing following trauma-hemorrhage (T-H). Androgen, ie, 5-dihydrotestosterone, is responsible for producing the depressed systemic cell-mediated immune responses following T-H in males. The aim of the present study was to determine whether depletion of 5-dihydrotestosterone in males before T-H has any salutary effects on wound immune cell function and wound healing in male mice following T-H.
Design: Mice were castrated or sham castrated 14 days before midline laparotomy (ie, tissue trauma) and subcutaneous polyvinyl sponge implantation, followed by hemorrhage (mean ± SEM blood pressure, 35 ± 5 mm Hg for 90 minutes and resuscitation) or sham operation. At 24 hours thereafter, wound immune cells from the sponges were harvested and cultured with lipopolysaccharide A. Release of interleukin 1 (IL-1) and IL-6 (in picograms per milliliter) was determined in the supernatants by enzyme-linked immunosorbent assay. In addition, IL-6 was assessed at the wound site by immunohistochemistry. Ten days after T-H, wound-breaking strength was measured.
Results: Precastration prevented the significantly suppressed capacity of wound immune cells to release IL-1 and IL-6. In addition, precastration normalized the elevated IL-6 expression at the wound site in the T-H mice. Moreover, wound-breaking strength was improved in castrated mice 10 days after T-H.
Conclusions: Male sex steroids appear to be responsible for wound immune cell dysfunction following trauma and severe blood loss. Because decreasing androgen levels resulted in improved wound healing, our results suggest that the use of androgen receptor–blocking agents, eg, flutamide, following T-H might represent a novel adjunct for decreasing the rate of wound complications under those conditions."
Complete study details and further references: http://archsurg.ama-assn.org/cgi/content/full/139/2/157
Also see: http://jcs.biologists.org/cgi/content/a ... cs.02786v1