DEHYDROEPIANDROSTERONE PROTECTS BOVINE RETINAL CAPILLARY PERICYTES AGAINST GLUCOSE TOXICITY

Pericyte loss is an early feature of diabetic retinopathy and represen ts a key step in the progression of this disease. This study aimed to evaluate the effect of dehydroepiandrosterone (DHEA) on glucose toxici ty in retinal capillary pericytes. Bovine retinal pericytes (BRP) were cultured in a high glucose concentration, with or without DHEA. After 4 days of incubation the number of BRP was significantly reduced by t he high glucose concentration. The addition of DHEA to the medium reve rsed the adverse effect of high glucose: BRP proliferation partially r ecovered in the presence of 10 nmol/l DHEA, and completely recovered i n the presence of DHEA at concentrations equal to or greater than 100 nmol/l. At physiological glucose concentrations, DHEA had no effect on BRP growth. Data show that DHEA, at concentrations similar to those f ound in human plasma, protects BRP against glucose toxicity. This effe ct seems specific for DHEA, since its metabolites, 5-en-androstene-3 b eta,17 beta-diol, dihydrotestosterone and estradiol did not alter BRP growth in normal or high glucose media. Various pieces of evidence lin k the antioxidant properties of DHEA to its protective effect on gluco se-induced toxicity in BRP.