TLR7在小鼠毛囊增值中作用的初步探讨

发布时间：2018-03-25 01:09

本文选题：TLR7　切入点：毛囊增值　出处：《重庆医科大学》2010年硕士论文

【摘要】： 研究目的:本课题基于前期研究发现TLR7受体在毛囊隆突部高表达并且给予TLR7激动剂咪喹莫特后小鼠毛囊数量增加及生长周期延长的发现拟通过RT-PCR的方法验证前期由基因芯片筛选出的可能的调控基因Fos,并通过使用JNK通路阻断剂SP600125在动物试验水平上进一步证实TLR7信号通路作用于毛囊干细胞的可能靶位基因,以期对TLR7信号通路对毛囊增殖调控的机制有初步的探讨。方法:6周大C57雌性小鼠10只,随机分为使用咪喹莫特实验组与使用生理盐水对照组。4周后小鼠背部皮肤取材,将所取皮肤组织TRIZOL法提取RNA,RT-PCR方法分析两组样品Fos基因mRNA的表达差异。再将C57雌性小鼠20只,随机分为咪喹莫特处理组、DMSO对照组、SP00125组和咪喹莫特及SP600125混合组,处理4周后各组小鼠背部皮肤HE染色观察组织学改变并行磷酸化组蛋白H3检测增殖情况。结果:(1) Fos mRNA在咪喹莫特实验组的表达率显著高于对照组,差异有统计学意义(P0.05)(2)阻断JNK信号通路后,再使用TLR7激动剂咪喹莫特,小鼠毛囊的增值水平较咪喹莫特处理组明显降低,但仍高于DMSO对照组。结论:(1)咪喹莫特可能通过激活TLR7使JNK通路下游基因FOS的活化来达到促进毛囊增值的作用。 (2)TLR7激活后可能通过JNK、NF-κB和IRF等多条信号通路共同作用达到促进毛囊增殖分化的效果。
[Abstract]:Objective: in this study, we found that TLR7 receptor was overexpressed in the protuberance of hair follicle and TLR7 agonist Imiquimod was given to the mouse hair follicle number and the growth cycle was prolonged. The results of this study are to be verified by RT-PCR method in the early stage of the study. The possible regulatory gene Foswas screened by gene chip, and the possible target gene of TLR7 signaling pathway acting on hair follicle stem cells was further confirmed by using JNK pathway blocker SP600125 in animal experiments. The aim of this study was to explore the mechanism of TLR7 signaling pathway regulating hair follicle proliferation. Methods Ten female C57 mice aged 6 weeks were randomly divided into two groups: the control group and the control group. The difference of mRNA expression of Fos gene between the two groups was analyzed by RT-PCR, and then 20 female C57 mice were randomly divided into two groups: Imiquimod treated group, DMSO control group, SP00125 group and imiquimod and SP600125 mixed group. After 4 weeks of treatment, HE staining was used to observe the histological changes and phosphorylated histone H3 was used to detect the proliferation of the dorsal skin of the mice in each group. Results the expression rate of Fos mRNA in Imiquimod group was significantly higher than that in control group (P 0.05). After blocking JNK signaling pathway, Imiquimod was used as a TLR7 agonist. The value-added level of mouse hair follicles was significantly lower than that of imiquimod treatment group, but still higher than that of DMSO control group. Conclusion Imiquimod may promote the proliferation of hair follicles by activating TLR7 and activating the downstream gene FOS of JNK pathway. The activation of TLR7 may promote the proliferation and differentiation of hair follicles through several signal pathways such as JNKN NF- 魏 B and IRF.
【学位授予单位】：重庆医科大学
【学位级别】：硕士
【学位授予年份】：2010
【分类号】：R758.7

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