| Research objectives: Our previous research found that TLR7 highly expressed in the hair follicle bulge. After using TLR7 agonist imiquimod, the number of hair follicles increased in mice, and extend the growth cycle. The basis of this subject in the preliminary work, further by RT-PCR method verified the possible regulation of gene Fos, and by using the SP600125 (JNK pathway inhibitor) in animal levels studies to further confirm and explore the role of TLR7 signaling pathway in hair follicle stem cells in the target gene view of the TLR7 signaling pathway on proliferation and regulation of hair follicle mechanism was discussed.Methods: 6-week-old C57 female mice, 10 mice were randomly divided into the use of imiquimod in the experimental group and control group using saline. Back skin of mice after 4 weeks were sacrificed to the TRIZOL extraction from skin tissue RNA, RT-PCR to analyze two samples of mRNA expression of Fos gene differences.Then 20 C57 female mice were randomly divided into treatment group imiquimod, DMSO control group, SP00125 group and imiquimod &SP600125 mixed group.4 weeks after treatment the skin of mice in each group H & E staining of histological change the parallel detection of phosphorylated histone H3 proliferation.Results: (1) Fos mRNA in the experimental group imiquimod significantly higher expression rate, the difference was statistically significant (P <0.05) (2) Block the JNK signaling pathway, then use the TLR7 agonist imiquimod, the proliferation level of mouse hair follicles than imiquimod treatment were significantly lower, but still higher than the DMSO control group.Conclusions: (1) imiquimod may activates TLR7 to enhance the proliferation of the follicle progenitor via Fos activities. (2) TLR7 may activates JNK,NF-κB and IRF several other channels to promote joint action of the effect of proliferation and differentiation of hair follicles. |