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Pulsed ultrasound regulates angiogenesis and vascular invasion of the osteochondral junction in arthritic knee cartilage
Author(s): 
Pages: 86-91
Year: Issue:  2
Journal: Chinese Journal of Physical Medicine and Rehabilitation

Keyword:  OsteoarthritisAngiogenesisVascular endothelial growth factorUltrasoundIntegrin β1;
Abstract: Objective To observe the effect of low-intensity pulsed ultrasound (LIPUS) on angiogenesis and vascular invasion in the osteochondral junctions of rabbits with osteoarthritis.Methods Eighteen 2 to 2.5 kg New Zealand rabbits were randomly divided into an early control group (EC),an early osteoarthritis group (EO) and an osteoarthritis plus LIPUS treatment group (ET),each of 6.The rabbits of the EO and ET groups received anterior cruciate ligament resection at their left hind limbs,while those of the EC group were sham-operated.The ET group was exposed to LIPUS radiation four weeks later when osteoarthritis had been established,while the EO and EC groups were exposed to fake LIPUS radiation.After four weeks of treatment the rabbits were sacrificed and pathological changes in the articular surface of the femoral condyle were assessed using Safranin O-fast green cartilage staining.Western blotting was used to examine the expression of integrin β1,p-FAK,p-JNK,p-p38,VEGF and chondromodulin-1(ChM-1).Results Compared with the EC group,significantly more angiogenesis and vascular invasion was observed in the osteochondral junctions of the EO and ET groups,with more vessels at the osteochondral junction and marked disorder of the tidal line broken up by vessels.The expression of integrin β1,p-FAK,VEGF,p-p38 and p-JNK was significantly higher in the EO group than in the EC group,while ChM-1 expression was significantly lower.Compared with the EO group,the expression of integrin β1,p-FAK and ChM-1 in the ET group was significantly higher,while that of VEGF,p38 and p-JNK was significantly lower.Conclusions LIPUS inhibited angiogenesis and vascular invasion in the osteochondral junctions of the osteoarthritie rabbits through activating an integrin β1-FAK-p38/JNK-VEGF/ChM-1 pathway.
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