Evaluation the effect of testosterone on the number of endothelial progenitor cells and amount of SDF-1α, PDGF, bFGF, and NO

Abstract

Background: Recent therapeutic advances in cardiovascular disease, thanks to the discovery of
endothelial progenitor cells (EPCs). Stromal cell‑derived factor‑1α (SDF‑1α), platelet‑derived
growth factor (PDGF), basic fibroblast growth factor (bFGF), and nitric oxide (NO) play a role
in migration, homing, and differentiation of EPCs into mature endothelial cells. The incidence of
cardiovascular disease is higher in men than in women. This fact suggests the influence of sex
hormones on incidence of cardiovascular disease.

Methods: Twenty‑four female wistar rats weighing
160–180 g were randomly divided into four groups (N = 6): 1. sham‑treated by sesame oil, 2.
ovariectomized (OVX)‑treated by sesame oil, 3. OVX‑treated by 10 µg/kg/day testosterone, and 4.
OVX‑treated by 100 µg/kg/day testosterone. After 21 days, the animals were euthanized and blood
samples were saved for determination of EPC count and serum levels of SDF‑1α, PDGF, bFGF,
and NO production.

Results: High‑dose testosterone induced significant increase in EPC count in
OVX rats (P ˂ 0.05). Also 100 µg/kg/day testosterone increased serum level of SDF‑1α more than
OVX‑treated by 10 µg/kg/day testosterone (P ˂ 0.05). But 10 µg/kg/day testosterone increased
significantly the serum level of PDGF >100 µg/kg/day testosterone‑treated group (P ˂ 0.05). The
serum level of bFGF in sham‑treated by sesame oil was equal with its concentration in OVX‑treated
by 100 µg/kg/day testosterone. And the serum concentration of NO production in testosterone‑treated
groups were significantly less than other groups (P < 0.05).

Conclusions: This study suggests that
testosterone might be effective on cardiovascular disease in females by increasing EPC count through
SDF‑1α and PDGF mechanisms which are some of the vascular healing factors.

Keywords: Basic fibroblast growth factor, endothelial progenitor cell, nitric oxide, platelet‑derived growth factor, stromal cell‑derived factor‑1α, testosterone