我们既往研究发现，雌激素受体α (ERα) 可以调节NLRP3炎症小体的表达及组装，而NLRP3炎症小体与脂肪肝的发生密切相关。另外我们发现植物雌激素染料木素（GEN）在蛋鸡脂肪肝出血综合征（FLHS）模型中具有良好的抗炎效果，但其作用机制未知。因此我们推测GEN可以通过靶向ERα-NLRP3信号通路抑制炎症反应，进而干预蛋鸡FLHS。本课题拟在建立蛋鸡FLHS模型和ERα、NLRP3敲低与过表达的原代鸡肝细胞脂肪变性模型的基础上，通过临床症状观察，生化指标分析，炎性因子和脂肪代谢因子分析，ERα表达及磷酸化检测，NLRP3炎症小体表达及组装检测，确定ERα、NLRP3对GEN干预FLHS的影响。进一步通过Co-IP、免疫荧光、GST pull-down、蛋白截短实验，探索ERα与NLRP3互作机制和结构域，最终阐明ERα靶向调控NLRP3炎症小体参与GEN缓解蛋鸡FLHS的作用机制。

In our previous research, we found that estrogen receptor α (ERα) could regulate the expression and assembly of NLRP3 inflammasome, and NLRP3 inflammasome was closely related to the occurrence of fatty liver. In addition, we found that phytoestrogen genistein (GEN) had a good anti-inflammatory effect on the fatty liver hemorrhage syndrome (FLHS) of the laying hens, however, its underlying mechanism is unknown. Based on this, we speculate that GEN can inhibit the inflammatory response through the ERα-NLRP3 signaling pathway, and then relieves FLHS in laying hens. Therefore, in this study, we plan to ascertain the influence of ERα and NLRP3 on GEN improved FLHS, through clinical symptoms observation, biochemical analysis, inflammatory factors and fat metabolism factors analysis, ER expression and phosphorylation detection, and NLRP3 inflammasome assembly analysis, using the constructed laying hens FLHS model, and ERα/NLRP3 knockdown and overexpression of primary hepatocyte steatosis model. Furthermore, Co-IP, immunofluorescence, GST pull-down, and protein truncation experiments will be used to explore the interaction between ERα and NLRP3. Finally, the mechanism of GEN on FLHS in laying hens via ERα-NLRP3 signaling pathway will be clarified.