前列腺组织炎症在BPH发生发展中的重要作用受到广泛关注，是当前研究BPH发病机制的热点。我们的前期研究发现：IL-2Rα在合并炎症的BPH上皮细胞中表达增高，IL-2可促进上皮细胞增殖并抑制其凋亡，提示IL-2可能是调控BPH组织炎症反应的重要因子。本项目拟在以上研究结果的基础上，应用RNAi和过表达技术改变IL-2Rα在前列腺上皮细胞中的表达，观察不同处理组中细胞增殖、凋亡及相关细胞因子分泌的情况，并检测信号通路JAK/STAT，Raf/MEK/ERK和PI-3K/Akt的激活情况；利用Cre/LoxP和来自酵母的FLP-frt系统构建特异性前列腺上皮细胞IL-2Rα表达缺失小鼠，建立炎症反应性BPH模型，观察IL-2Rα表达缺失对BPH病理生理特征、前列腺细胞增殖、凋亡及相关细胞因子的影响。本研究将初步阐明IL-2/IL-2R通路在BPH组织炎症中的调控机制，为BPH的防治拓展新思路。

Histological inflammation in the development of benign prostatic hyperplasia (BPH) has attracted widespread attention and also a hot-spot in current researches. In our previous study, we found IL-2α expression was associated with inflammatory pathology in BPH, IL-2 could activate ERK1/2 pathway leading to proliferation of BPH-1 cells and protect these cells against apoptosis. On the basis of the above findings, we plan to use overexpression and RNAi suppression of the IL-2Rα gene in BPH-1 cells, observe the cell proliferation, apoptosis and related cytokines secretion. Meanwhile detect the activation states of JAK/STAT, Raf/MEK/ ERK and PI-3K/Akt signaling pathways. We plan to develop IL-2Rα-deficient mice using the Cre/LoxP and FLP-frt recombination systems, observe the influence of IL-2Rα deficiency on histology of prostate lesions, cell proliferation, apoptosis and related cytokines secretion. The study will initially clarify the role of IL-2/IL-2R pathway in the regulatory mechanism of BPH tissue inflammation, offer new therapeutic options for BPH.