回医烙灸通过Fas/FasL通路干预激素性股骨头坏死的机制研究

激素导致骨细胞、成骨细胞凋亡增加和破骨细胞凋亡的寿命延长是SANFH和缺血性骨坏死的细胞学基础。特色回医烙灸疗法治疗早期SANFH临床疗效确切，能减少缺血性骨坏死，但作用机制不明。前期研究发现，回医烙灸可减少SANFH大鼠模型成骨细胞的凋亡及骨组织中IL-1和Caspase-3的表达，而IL-1和Caspase-3是Fas/FasL通路上下游的关键作用因子，激活该通路可增加成骨细胞的凋亡，因此提出回医烙灸可能是通过Fas/FasL通路调控SANFH骨代谢的假说。本课题采用回医烙灸干预大鼠SANFH模型，研究回医烙灸通过Fas/FasL通路对成骨、破骨和骨细胞增殖及凋亡的调节机制；探讨回医烙灸通过Fas/FasL通路对成骨、破骨和骨细胞外基质环境的调控机制，从而验证回医烙灸可能介导Fas/FasL通路调控SANFH骨代谢的假说，阐明其部分作用机制，为回医烙灸治疗SANFH提供理论和实验依据。

Hormone leads to bone and osteoblast apoptosis increase and Osteoclast apoptosis extension as a cytological basis for steroid-induced femoral head necrosis (SANFH) and ischemic osteonecrosis.In Hui medicine,cautery moxibustion is one of the most effective treaments to SANFH and can reduce ischemic osteonecrosis, but the mechanism of action is unknown.In our previous studies on rats,we have found that cautery moxibustion therapy can reduce the apoptosis of osteoblasts and the expression of Caspase-3 and the IL-1 in the femoral-head.While IL-1 and Caspase-3 are key factors of the Fas/FasL signal pathways,and activating this pathway can increase the apoptosis of osteoblasts. Therefore the hypothesis that the cautery moxibustion possibly treats SANFH through mediating the Fas/FasL signaling pathway is proposed.In this study the model of cautery moxibustion intervention of rats，SANFH is adopted.Reseach contents:1.The mechanism of the cautery moxibustion influence multiplication and apoptosis of bone cells through mediating the Fas/FasL signaling pathway;2.The mechanism of the cautery moxibustion regulate the extracellular matrix of bone cells through mediating the Fas/FasL signaling pathway.The purpose of the study is to testify the hypothesis that the cautery moxibustion may treat SANFH through mediating Fas/FasL signaling pathway.