Prednisone blocks Peripheral blood lymphocytes (PBL) growth in the G1 phase of cell cycle and inhibits both IL-2 receptor (IL-2R) expression and IL-2 secretion in activated human peripheral blood T lymphocytes. Prednisone increases apoptosis in PHA-activated human PBL, and the apoptotic effect of Prednisone is stronger on CD8(+) than on CD4(+) T lymphocytes. [1]

Prednisone-treated rats show a significant delay of 20% in learning and memory retention in rats as compared with controls. [2] Prednisone results in reduced weight gain, unchanged alter uterine weight, lowered serum magnesium (Mg), unchange serum calcium (Ca), phosphate (P), 25-hydroxyvitamin D (25OHD), or 1,25-dihydroxyvitamin D [1,25(OH)2D], striking increased in calcified cartilage, reduced cross-sectional area and cortical area, unchange medullary area of the tibial diaphysis, lowered periosteal and endocortical bone formation and apposition rates, increased mean cancellous bone area and cancellous bone perimeter of the tibial metaphysis in both sham-operated and ovariectomized rats. [3] Prednisone-treated rabbit shows a 30% reduction in percent stenosis, a 35% decrease in neointimal area, and a 66% decrement in neointimal thickness. [4] Prednisone treatment significantly reduces the level of TGF-beta1 and HYP in diaphragm from mdx mice to values similar to control mice, but results in a higher level of the HP cross-link compared with untreated mdx mice. [5]