Hu Tianyong, Hu Wenhui, Ma Li, Zeng Xianhai, Liu Jiangqi, Cheng Baohui, Yang Pingchang, Qiu Shuqi, Yang Gui, Chen Donghui, Liu Zhiqiang
Longgang ENT Hospital, Institute of ENT and Shenzhen Key Laboratory of ENT, Shenzhen, China.
Zunyi Medical College, Zunyi, China.
Dig Liver Dis. 2019 Jun;51(6):790-797. doi: 10.1016/j.dld.2018.11.005. Epub 2018 Nov 17.
To investigate whether the intrarectal administration of the ubiquitin E3 ligase A20 (A20) attenuates intestinal inflammation and influences regulatory T cells in experimental colitis.
A dextran sulfate sodium induced chronic colitis mouse model was established. The symptoms and manifestations of colitis and the severity of colonic mucosal inflammation were evaluated. The protective role of A20 expression in the intestine was analyzed after the administration of a pVAX1-A20 recombinant eukaryotic vector, which was encapsulated into poly(L-lactide-co-glycolide) as a nanoparticle.
pVAX1-A20 administration markedly ameliorated colonic tissue damage and reduced intestinal inflammation via the suppression of the mucosal mitogen-activated protein kinase and nuclear factor (NF)-κB signaling cascade. Furthermore, pVAX1-A20 promoted the splenic regulatory T cell population and forkhead box P3 expression in colonic tissue.
A20 plays a key role in the regulation of intestinal inflammation and that the overexpression of A20 in the intestine protects mice from dextran sulfate sodium induced chronic colitis.
研究直肠内给予泛素E3连接酶A20（A20）是否能减轻实验性结肠炎中的肠道炎症并影响调节性T细胞。
建立葡聚糖硫酸钠诱导的慢性结肠炎小鼠模型。评估结肠炎的症状和表现以及结肠黏膜炎症的严重程度。在将pVAX1-A20重组真核载体封装成纳米颗粒形式的聚（L-丙交酯-共-乙交酯）后给予小鼠，分析A20在肠道中的表达所起的保护作用。
给予pVAX1-A20通过抑制黏膜丝裂原活化蛋白激酶和核因子（NF）-κB信号级联反应，显著改善结肠组织损伤并减轻肠道炎症。此外，pVAX1-A20促进了脾脏调节性T细胞群体以及结肠组织中叉头框P3的表达。
A20在肠道炎症调节中起关键作用，且肠道中A20的过表达可保护小鼠免受葡聚糖硫酸钠诱导的慢性结肠炎。
