目的 探讨脂钙蛋白2（lipocalin2， LCN2）调控表皮生长因子受体（epidermal growth factor receptor， EGFR）磷酸化对人输卵管炎性上皮细胞损伤的影响。 方法 取人输卵管上皮细胞，LPS干预建立细胞模型，随机分为空白对照（Control）组、模型（Model）组、实验（Model + si-LCN2或Model + oe-LCN2）组和阴性对照（Model + si-NC或Model + oe-NC）组。探究细胞活性、细胞凋亡、细胞炎症水平、EGFRmRNA、LCN2、EGFR、p-EGFR、p-EGFR/EGFR蛋白表达水平变化。 结果 与Model组相比，Model+si-LCN2组细胞活性提升、细胞凋亡率减低，炎症因子表达下降（P < 0.05）；免疫共沉淀证实LCN2与EGFR存在靶向关系。与Model组相比，Model + oe-LCN2组p-EGFR、p-EGFR/EGFR水平升高（P < 0.05），EGFR改变不大（P > 0.05）。 结论 抑制LCN2所介导的EGFR磷酸化，可提高细胞活性、减轻细胞凋亡及细胞炎症，从而改善LPS诱导的人输卵管上皮细胞炎性损伤。

Objective To investigate the regulatory effect of lipocalin 2 （LCN2） on epidermal growth factor receptor （EGFR） phosphorylation and its impact on inflammatory damage in human fallopian tube epithelial cells. Methods Human fallopian tube epithelial cells were isolated and a lipopolysaccharide （LPS） intervention was applied to establish an in vitro cell model. The cells were randomly assigned into the following groups： a blank control group （Control）， a model group （Model）， experimental groups （Model + si-LCN2 or Model + oe-LCN2）， and negative control groups （Model + si-NC or Model + oe-NC）. Changes in cell viability， apoptosis rates， inflammatory levels， as well as the expression of EGFR mRNA， LCN2， EGFR， p-EGFR， and the ratio of p-EGFR/EGFR proteins were evaluated. Results Compared to the Model group， the Model + si-LCN2 group exhibited enhanced cell viability， a reduced apoptosis rate， and decreased expression of inflammatory factors （P < 0.05）. Immunoprecipitation analysis confirmed a direct interaction between LCN2 and EGFR. In comparison with the Model group， the Model + oe-LCN2 group demonstrated elevated levels of p-EGFR and the p-EGFR/EGFR ratio （P < 0.05）， while no significant change was observed in total EGFR expression （P > 0.05）. Conclusion Inhibition of LCN2-mediated EGFR phosphorylation enhances cell viability， reduces apoptosis， and mitigates inflammatory responses， thereby ameliorating LPS-induced inflammatory injury in human fallopian tube epithelial cells.