Dehydroepiandrosterone protects the microcirculation of muscle flaps from ischemia-reperfusion injury by reducing the expression of adhesion molecules.

Adhesion molecules contribute to ischemia-reperfusion injury by increasing the endothelial adhesion and extravasation of leukocytes. Scientific evidence suggests that presurgical treatment with dehydroepiandrosterone may protect the microvasculature against this damage, but the exact mechanism is not known. The purpose of this study was to investigate the effects of presurgical dehydroepiandrosterone treatment on microcirculatory hemodynamic parameters and the expression of adhesion molecules in a rat cremaster muscle flap model.

Effect of subepineurial dehydroepiandrosterone treatment on healing of transected nerves repaired with the epineurial sleeve technique.

The epineurial sleeve technique for nerve repair is designed in part to protect a healing nerve from external humoral influences, but research suggests that the external factor dehydroepiandrosterone (DHEA) may actually improve nerve healing in crush injuries. To test the effect of DHEA, we injected it into the epineurial chambers created to repair transected rat sciatic nerves. In 18 control rats, the nerve was transected and repaired without DHEA treatment.

DNA immunization utilizing a herpes simplex virus type 2 myogenic DNA vaccine protects mice from mortality and prevents genital herpes.

A gene transfer vector for DNA immunization was developed in which the promoter was derived from the murine muscle creatine kinase (MCK) gene; a gene expressed only in differentiated skeletal muscle. In vitro, we observed high-level, but unrestricted, gene expression from the cytomegalovirus (CMV) promoter unlike expression from the MCK promoter which was weak but restricted to myofibers. A myogenic DNA vaccine (MDV) that encoded the glycoprotein D gene from herpes simplex virus type-2 (HSV-2) was used to DNA immunize mice.

Anti-interleukin-6 antibodies inhibit herpes simplex virus reactivation.

Herpes simplex viruses (HSVs) infect epithelial cells, become localized in neurons, and can reactivate in response to a variety of stimuli, including ultraviolet light and hyperthermia. The sequence of gene activation during viral replication is known, but the molecular linkage between exogenous stimuli and HSV reactivation has not been determined. It was hypothesized that interleukin (IL)-6 acts as a signal between exogenous stimuli and neurons, stimulating HSV reactivation from latency.

Administration of dehydroepiandrosterone sulfate retards onset but not progression of autoimmune disease in NZB/W mice.

NZB/W mice spontaneously develop an autoimmune disease characterized by the formation of anti-DNA antibodies and subsequent development of a fatal immune complex-mediated glomerulonephritis. Treatment of NZB/W F1 female mice with DHEAS, a precursor of DHEA, beginning at 2 months of age delayed the onset of autoimmune disease and prolonged survival. Animals treated with DHEAS beginning at 2 months of age had significantly lower anti-dsDNA serum antibody titers when compared to controls.