反式玉米素抑制紫外线诱导的水通道蛋白3下调有关的信号通路  

Trans-Zeatin inhibits the signal pathway of UV-induced AQP3 downregualtion

作　　者：蒋洁瑶[1] 纪超[1] 毕志刚[2] 张美华[1] 

机构地区：[1]南京医科大学第一附属医院皮肤性病科,江苏南京210029 [2]南京医科大学附属明基医院皮肤科,江苏南京210019

出　　处：《临床皮肤科杂志》2013年第6期342-344,共3页Journal of Clinical Dermatology

基　　金：国家自然科学基金(810701297和81101188)资助项目

摘　　要：目的:观察能特异性诱导水通道蛋白-3(AQP3)表达的反式玉米素(trans-zeatin,tZ)对紫外线导致的AQP3丢失的影响及PD98059、U0126和MEK/细胞外信号调节激酶(ERK)抑制剂对紫外线引起的AQP3丢失的作用。方法:蛋白质免疫印迹方法分析各蛋白的表达。结果:tZ抑制了紫外线诱导的MEK/ERK活化,后者作为关键信号通路调节由紫外线诱导的AQP3丢失。tz的预处理很大程度上抑制了MEK的磷酸化,且具有剂量-效应关系。MEK/ERK的抑制剂PD98059和U0126抑制紫外线引起的AQP3下调,而c-Jun氨基端激酶(JNK),P38或丝氨酸/苏氨酸蛋白激酶(AKT)的抑制剂则没有抑制效应。结论:tZ对抗紫外线引起AQP3丢失的保护作用是由抑制紫外线引起的MEK/ERK活化介导的。Objective： To observe the effects of Trans-Zeatin （TZ）, which specifically induces AQP3 expression, on UV-in- duced loss of AQP3 and to evaluate the inhibitory effects of PD98059, U0126 and MEK/ERK inhibitors on UV-induced loss of AQP3. Methods： Western blot was used to assess the effects of PD98059 U0126, and MEK/ERK inhibitors on MEK/ERK activation and protein expression. Results： TZ inhibited UV-induced MEK/ERK activation was found; the latter served as a key signal pathway mediating UV-induced AQP3 loss. Pretreatment with TZ largely inhibited UV-induced MEK phosphoryla- tion in a dose-dependent manner. PD98059 and U0126, the inhibitors of MEK/ERK but not JNK, p38 or AKT inhibitors, in- hibited UV-induced AQP3 down-regulation. Conclusions： The protective effect of TZ against UV-induced loss of AQP3 is mediated, at least in part, by its inhibitory effect on UV-induced MEK/ERK activation.

关 键 词：反式玉米素 水通道蛋白3 MEK ERK MEK ERK抑制剂 

分 类 号：R339.57[医药卫生—人体生理学]