Hui Medicine Moxibustion Improves Steroid-Induced Avascular Necrosis of the Femoral Head in Rats via Down-Regulating Fas/Fasl Signal Pathway

Background: Our previous study has shown that Hui Medicine moxibustion (HMm) can improve the steroid-induced avascular necrosis of the femoral head (SANFH) at the early stage. The primary purpose of this study was to explore the therapeutic effect and underlying molecular mechanisms of HMm treatment in rats with SANFH.Methods: We established SANFH rat models, which were treated with HMm alone and with Fas activating antibody. Hema-toxylin and eosin (H&E) staining was applied to assess the effects of HMm intervention on the altered pathological features of subchondral bone. Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining, western blotting, immuno-histochemistry, and RT-PCR were performed to detect the expression of proteins related to Fas-mediated apoptosis.Results: We found that HMm treatment significantly reduced bone resorption, damage, and loss of subchondral bone. Cell apoptosis in trabecular bone and marrow significantly decreased in Hui/SANFH group after treatment for four weeks with HMm. Compared to the SANFH group, the levels of Fas, FasL, FADD, c-Caspase-8, and c-Caspase-3 dramatically reduced in the Hui/SANFH group. However, HMm intervention significantly decreased the mRNA levels of MMP-1 and MMP-3. Also, it increased Runx-2 expression and the ratio of OPG/RANKL, whereas the anti-Fas antibody treatment abolished the effect of HMm intervention.Conclusions: The study strongly demonstrates for the first time that HMm treatment may play an important role in improving SANFH via downregulating the Fas/FasL signal pathway.

Automated summary

HMm treatment significantly reduced bone resorption, damage, and loss of subchondral bone in SANFH rats. It also decreased cell apoptosis, downregulated Fas/FasL signal pathway, and increased Runx-2 expression, suggesting its potential therapeutic effect on SANFH.