Objective   To investigate the effects of ALT711 intervention on the activity of bone marrow-derived endothelial progenitor cells (EPCs) for the purpose of exploration of the possible mechanisms in fu

nctional changes of EPCs due to ALT711-mediated age-related impairment and the roles of ALT711 in the repair and regeneration of the damaged vessels.   Methods   ALT711 (1 mg·kg

-1

·d

-1

) was feed to 3-4

10-12 and 18-20 month old rats. After 4 weeks of feeding

rats were sacrificed and mononuclear cells were obtained from the bone marrow. Mononuclear cells were cultured with medium DMEM for 7 d. EPCs were identified as adherent cells double-positive stained for FITC-UEA-I and DiI-acLDL by laser confocal microscopy. A modified Boyden’s chamber was used to assess the migration of EPCs and the number of the recultured EPCs was counted for the measurement of the adhesion function. A spectrophotometer was used to determine the proliferation function. Sera from different aged rats were collected and used to culture EPCs from 3-4 month old rats in the absence or presence of ALT711 (20  μg/ml). At 7 d after culture

the migration

adhesion and proliferation functions of EPCs were detected.   Results   The functional activities of EPCs could be the hallmark of aging. ALT711 feeding released aging impaired proliferation

migration and adhesion of EPCs. Aged rat serum partially inhibited the activity of EPCs in young rats

but ALT711 intervention could block this effect.   Conclusion   ALT711 can mediate age-related impairment of progenitor cell function and block the harmful effect on aged rat serum

which indicates a new pathophysiological mechanism in atherosclerosis and suggests a new way of progenitor cell therapy.