JNK在牙囊细胞破骨细胞向分化的实验研究

Abstract

Abstract: Objective　 To investigate the mechanism of JNK signaling in the formation of mature osteoclasts during tooth eruption in rats by inhibiting the JNK signaling pathway with the specific inhibitor SP600125. Methods SD rat dental follicle cells were isolated and cultured. Different concentrations of SP600125 were used to pretreat cells. Real-time quantitative PCR was used to detect the expressions of nuclear factor κB receptor activator ligand and osteoprotegerin gene in DFCs. DFCs and BMMs established a co-culture system and TRAP staining was used to observe the amount of OC. Results SP600125 had no significant effect on the proliferation of DFCs under the concentration range of 20 μmol/L (P>0.05). RT-PCR results showed that after 72 hours of SP600125 intervention, the expression of RANKL gene decreased while that of OPG increased. There were statistical differences compared with the control group (P<0.05). Positive TRAP staining results showed that OC was generated in each group, and the number of OC generated on the 9th day significantly increased compared to the 7th day. The number of osteoclasts decreased in the inhibitor group under different concentrations, and the difference was statistically significant compared with the control group (P<0.05). Conclusion This study clarifies that in rat tooth eruption, SP600125 in some degree inhibits the formation of OC by inhibiting the JNK signaling pathway, which can provide a researh basis for the study of tooth eruption, alveolar bone remodeling and other osteoclast-related oral diseases.

Key words: tooth eruption, osteoclast, c-Jun terminal kinase, nuclear factor κB receptor activator ligand, osteoprotegerin

CLC Number:

R329.28

References

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An experimental study on JNK differentiation of osteoclast cells in dental foam cells

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