11β-hydroxysteroid dehydrogenases as targets in the treatment of steroid-associated femoral head necrosis using antler extract.

The aim of the present study was to investigate the therapeutic effect of deer antler extract on avascular necrosis of the femoral head (ANFH) induced by steroids, and to confirm that 11β-hydroxysteroid dehydrogenases (11β-HSD) are one of the targets of treatment with antler extract. A total of 30 rabbits were randomly divided into 5 groups (n=6): A control, ANFH, ANFH + antler (250 mg/kg), ANFH + antler (500 mg/kg) and ANFH + antler (1,000 mg/kg) group. Rabbits in the experimental groups were injected with methylprednisolone and horse serum to establish a steroid-induced ANFH (SANFH) model. Rabbits in the ANFH + antler (250 mg/kg), ANFH + antler (500 mg/kg) and ANFH + antler (1,000 mg/kg) groups were treated with intraperitoneal injection of 250, 500 or 1,000 mg/kg antler extract/day, respectively, for 60 days. Serum samples were then extracted to determine total cholesterol (CT) and triglyceride levels, treat osteoblasts, measure 11β-HSD (11β-HSD1) and 11β-HSD2 and alkaline phosphatase (ALP) levels and cellular apoptosis, and determine the proportion of osteoblasts in each phase of the cell cycle. Serum CT and triglyceride levels in SANFH rabbits significantly decreased as the concentration of antler increased (P<0.05). 11β-HSD1 levels in the femoral heads of SANFH rabbits and osteoblasts following treatment with antler-containing serum decreased as the concentration of antler used increased, whereas levels of 11β-HSD1 increased significantly (P<0.05). The proliferation of osteoblasts and ALP levels in osteoblasts increased as the antler concentration increased, whereas the number of osteoblasts in the G0/G1 phase decreased significantly (P<0.05). The current study demonstrated that treatment with antler extract has a therapeutic effect on ANFH induced by steroids in rabbits and may regulate the expression of 11β-HSD in femoral heads and osteoblasts, as well as promoting the proliferation of osteoblasts.