Naringin protects against steroid­induced avascular necrosis of the femoral head through upregulation of PPARγ and activation of the Notch signaling pathway.

Naringin, a flavonoid, is the effective pharmaceutical ingredient of drynaria, with the effects of healing fractures, strengthening bones and promoting kidney function. The aim of the present study was to investigate the potential effect of naringin on steroid­induced avascular necrosis of the femoral head (SANFH). Treatment with naringin markedly protected against the steroid­induced decrease in serum osteocalcin levels, and the rate of osteonecrosis in a model of SANFH. In addition, naringin decreased the total cholesterol and low density lipoprotein/high density lipoprotein ratio in the SANFH rabbit. It was observed that naringin markedly inhibited caspase­3 activity, increased runt­related transcription factor 2 and transcription factor sp7 mRNA expression, promoted alkaline phosphatase activity and upregulated collagen I, peroxisome proliferator­activated receptor (PPAR) Î³2, neurogenic locus notch homolog protein (Notch), ß­catenin and phosphorylated­Rac­α serine/threonine protein kinase protein expression in the SANFH rabbit. The results of the present study demonstrated that naringin protects against SANFH through upregulation of PPARγ2 and activation of the Notch signaling pathway, and may be a useful addition to the treatment options for diseases of the femoral head.

Repairing cartilage defects using chondrocyte and osteoblast composites developed using a bioreactor.

BACKGROUND: Articular cartilage injury is a common disease, and the incidence of articular wear, degeneration, trauma and sports injury is increasing, which often lead to disability and reduced quality of life. Unfortunately repair of articular cartilage defects do not always provide satisfactory outcomes. METHODS: Chondrocyte and osteoblast composites were co-cultured using a bioreactor. The cartilage defects were treated with cell-ß-tricalcium phosphate (ß-TCP) composites implanted into osteochondral defects in dogs, in vivo, using mosaicplasty, by placing chondrocyte-ß-TCP scaffold composites on top of the defect and osteoblast-ß-TCP scaffold composites below the defect. RESULTS: Electron microscopy revealed that the induced chondrocytes and osteoblast showed fine adhesive progression and proliferation in the ß-TCP scaffold. The repaired tissues in the experimental group maintained their thickness to the full depth of the original defects, as compared with the negative control group (q = 12.3370, P < 0.01; q = 31.5393, P < 0.01). CONCLUSIONS: Perfusion culture provided sustained nutrient supply and gas exchange into the center of the large scaffold. This perfusion bioreactor enables the chondrocytes and osteoblasts to survive and proliferate in a three-dimensional scaffold.