基于PPAR/NF-κB信号通路探讨蛇床子素通过抑制IL-31干预特应性皮炎慢性瘙痒的机理研究

特应性皮炎（AD）是常见的慢性瘙痒病。IL-31是引起AD瘙痒的关键因子。抑制IL-31可减轻瘙痒。过氧化物酶体增殖物激活受体（PPAR）是一种参与皮肤功能的转录因子，激活PPAR可调节AD的细胞因子。NF-κB信号通路是AD的重要通路，激活PPAR可阻断NF-κB通路。蛇床子是广西常用止痒壮药，本组前期研究表明蛇床子成分蛇床子素（Osthole）抑制AD的IL-31。但是，Osthole通过何种信号通路与分子抑制IL-31干预AD慢性瘙痒，尚不清楚。课题组提出“Osthole通过激活PPAR与抑制NF-κB信号通路调节IL-31干预AD慢性瘙痒”的理论假说。研究将运用动物与细胞模型，采用行为学、ELISA、RT-PCR、Western Blot、组化等方法，观察Osthole抑制AD小鼠IL-31干预慢性瘙痒的分子机制。研究将为临床上运用Osthole治疗慢性瘙痒提供更多的实验依据。

Atopic dermatitis (AD) is a normal chronic pruritus disease. IL-31 play a key role in the chronic itch of AD. Itch was inhibited by reduced IL-31. Peroxisome proliferators-activated receptor (PPAR) is involved in the functional role of skin. NF-κB signal pathway is an important pathway which is blocked by activated PPAR. The fruit of Cnidium monnieri is a commonly used anti-itch traditional herb of ZHUANG. Previous studies showed that osthole, the main component of Cnidium monnieri, decrease IL-31 in AD mice. However, how osthole decrease IL-31 and inhibit chronic pruritus of AD is unclear. We proposed that osthole decrease IL-31 of AD by activated PPAR and inhibited NF-κB signal pathway. Animal model of AD, mast cell and keratinocytes lines were applied in this study. Behavior test, ELISA, RT-PCR, Westen Blot and histochemistry methods were used to observe the antipruritic mechanism of osthole on inhibition of IL-31. All above studies will provide more experimental evidence for the clinical application of osthole in the treatment of chronic pruritus.