摘要
目的:腋臭是美容整形外科的常见病,目前发病机制尚不明确,已证实人体大汗腺中的载脂蛋白D(ApoD)在腋臭患者大汗腺中高表达,并且与腋臭的发生密切相关。探明ApoD在大汗腺细胞中的信号转导通路,可以进一步明确其在腋臭发病过程中的作用机制。JNK信号转导通路与多种疾病的发生有关。课题组前期已经做了JNK1对ApoD调控作用的相关研究,证明了在腋臭发病过程中JNK1是通过调控ApoD的转录来上调ApoD的表达。本实验在课题组前期研究基础上,探讨JNK1下游转录因子AP-1是否在JNK1上调ApoD通路中发挥作用。方法:取腋臭志愿者腋区皮肤组织,进行汗腺细胞培养。把汗腺细胞分为5-二氢睾酮处理组、5-二氢睾酮联合姜黄素处理组和空白对照3个组,用姜黄素抑制AP-1的活性,通过Real-time PCR实验方法检测ApoD在姜黄素抑制下的表达变化。结果:在姜黄素的抑制下,ApoD表达明显降低。在体外培养汗腺细胞加入5-二氢睾酮联合姜黄素处理后,ApoD的表达量在mRNA水平低于单独的5-二氢睾酮处理组和正常对照组(P<0.05)。结论:姜黄素抑制了AP-1的活化导致ApoD的表达降低。在腋臭的发病过程中,JNK1的下游转录因子AP-1对ApoD有明显的上调作用。AP-1可能在JNK1上调ApoD这条通路中扮演了很重要的角色,它可能是JNK1和ApoD的中间转录因子。
Objective： Axillary osmidrosis is a common disease in plastic surgery which pathogenesis is not clear at present. It has been proved that ApoD was highly expressed in the sweat gland of axillary osmidrosis patient and closely related to this disease. We can further clarify the pathogenesis of axillary osmidrosis through verify the signal transduction pathway of ApoD in the sweat gland cells. JNK signal transduction pathway is related with many diseases.We have done the research work about JNK1 on the regulation of ApoD, and proved that JNK1 upregnlation of ApoD through regulation transcriptional of ApoD in the pathogenesis of axillary osmidrosis .On the basis of previous experiment of our research group, furthermore, we study on the effect of AP-1 （Downstream transcription factor of JNK1） in the pathogenesis of axillary osmidrosis. Methods： Sweat gland cells culture used the intact skin of underarm area. The sweat gland cells were divided into -dihydrotestosteron~ treatment group, 5 -dihydrotestosterone combined with curcumin treatment group and blank control group. The activity of AP-1 was inhibited by Curcumin, and the expression change of ApoD was detected by Western blot- ting and Real-time PCR. Results： Under the inhibition of Curcumin, the expression of ApoD was significantly lower. Sweat gland cells in vitro cultured using 5-dihydrotestosterone combined with Curcumin treatment, the expression of ApoD mRNA is lower than the other two groups （P〈0.05）. Conclusion： Curcumin inhibited the activation of AP-1, and the expresstion of ApoD was depressed. The ex- presstion of ApoD was upregnlated by AP-1 （Downstream transcription factor of JNK1） in the pathogenesis of axillary osmidrosis. AP-1 may play an important role in the up-regulation of JNK1 ApoD pathway, which may be an intermediate transcription factor between JNK1 and ApoD.
出处
《现代生物医学进展》
CAS
2013年第27期5251-5254,共4页
Progress in Modern Biomedicine
基金
国家自然科学基金项目(81271579)
陕西省社会发展攻关计划项目(2012K16-12-01)
关键词
腋臭
载脂蛋白D
JNK
AP-1
转录调控
Axillary osmidrosis
Apolipoprotein D（ApoD）
c-Jun N-teminal Kinase （JNK）
Activator protein-1
Transcriptional con-trol
