通过抑制Toll样受体3途径的体外和体内，emodin对手，脚和口腔疾病的Coxsackievivirus B3M介导的脑炎的作用。
abraction：
j Infect dis。 2020年7月6日； 222（3）：443-455。 PMID： 32115640“> 32115640 You-Qin Wang, Hui Li, Yu Li, Jing-Yu Ji, Ji-Hong Zhang, Lei Zhao
Article Affiliation:Yan Ding
Abstract:BACKGROUND: Encephalitis in hand, foot, and mouth disease (HFMD) is a serious threat to childrens health and 生活。 Toll样受体3（TLR3）是一种先天免疫识别受体，可以识别病毒并启动先天免疫反应。 EMODIN具有抗炎和调节免疫功能的作用，但是机制不是很清楚。
METHODS: Cells and mice were pretreated with coxsackievirus B3m (CVB3) and treated with emodin. The messenger ribonucleic acid (mRNA) and protein levels of TLR3 and downstream molecules were detected by quantitative real-time polymearse chain reaction and western blotting analysis, respectively. TLR3 expression was also downregulated by抗TLR3抗体（TLR3AB）或小型干扰（siRNA）使用苏木精和曙红染色评估。免疫吸附测定。
结果： emodin降低了TLR3的mRNA和蛋白质水平，并在下调tlr3级别的体外和下游分子降低了tlr3和sirna reterne sirnna and ottraine and sirnna and sirnna and sirnna and simod，TLR3和下游分子。 Emodin还对病理学，脑组织中的TLR3蛋白以及IL-6，NF-κB，IFN-β的表达显示出显着影响TLR3途径。