目的 观察栀子苷（geniposide, GE）对脂多糖（lipopolysaccharide, LPS）诱导的人冠状动脉内皮细胞（human coronary artery endothelial cell, HCAEC）炎症损伤的作用及机制。 方法 将HCAEC随机分为4组：对照组不予处理，模型组给予LPS（20 ng/mL）处理24 h，GE组给予GE（30 μg/mL）预处理12 h后使用LPS（20 ng/mL）处理24 h，沉默信息调节因子3（silent information regulaton 3, SIRT3）抑制剂组给予GE（40 μg/mL）与SIRT3特异性抑制剂3⁃TYP共同预处理12 h后使用LPS（20 ng/mL）处理24 h。采用CCK⁃8法检测细胞活力，试剂盒检测细胞培养基中乳酸脱氢酶（lactate dehydrogenase, LDH）活性及细胞中丙二醛（malondialdehyde, MDA）、谷胱甘肽（glutathione, GSH）、亚铁离子（Fe²⁺）水平，DCFH⁃DA荧光探针法检测活性氧（reactive oxygen species, ROS）水平，Western blot法检测SIRT3、谷胱甘肽过氧化物酶4（glutathuone peroxidase 4, GPX4）、溶质载体家族7成员11（solute carrier family 7 member 11, SLC7A11）、转铁蛋白受体1（transferrin receptor 1, TfR1）蛋白表达水平，免疫荧光染色检测SIRT3表达。 结果 与对照组相比，模型组细胞活力、GSH含量、SIRT3荧光强度及GPX4、SLC7A11、SIRT3蛋白表达降低（P<0.05），LDH活性、TfR1蛋白表达及MDA、Fe²⁺、ROS含量升高（P<0.05）；与模型组相比，GE组细胞活力、GSH含量、SIRT3荧光强度及GPX4、SLC7A11、SIRT3蛋白表达升高（P<0.05），LDH活性、TfR1蛋白表达及MDA、Fe²⁺、ROS含量降低（P<0.05）；与GE组比较，SIRT3抑制剂组细胞活力、GSH含量、SIRT3荧光强度及GPX4、SLC7A11、SIRT3蛋白表达降低（P<0.05），LDH活性、TfR1蛋白表达及MDA、Fe²⁺、ROS含量升高（P<0.05）。 结论 GE可改善LPS诱导的HCAEC炎症损伤，其机制可能与抑制细胞铁死亡及激活SIRT3信号通路有关。

Objective To study the effect and mechanism of geniposide (GE) on lipopolysaccharide (LPS)-induced inflammatory injury in human coronary artery endothelial cells (HCAECs). Methods HCAECs were randomly assigned to four groups: control (no treatment); model (LPS 20 ng/mL for 24 hours); GE (GE 30 μg/mL pretreatment for 12 hours, followed by LPS 20 ng/mL for 24 hours); and SIRT3 inhibitor (GE 40 μg/mL plus the SIRT3-specific inhibitor 3-TYP pretreatment for 12 hours, followed by LPS 20 ng/mL for 24 hours). Cell viability was assessed by CCK-8 assay. Lactate dehydrogenase (LDH) activity in culture medium and intracellular malondialdehyde (MDA), glutathione (GSH), and ferrous ion (Fe²⁺) levels were measured using commercial kits. Reactive oxygen species (ROS) were evaluated by DCFH-DA fluorescent probe method. Western blotting detected the protein expression of silent information regulator 3 (SIRT3), glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), and transferrin receptor 1 (TfR1). SIRT3 expression was examined by immunofluorescence staining. Results Compared with the control group, the model group showed decreased cell viability, GSH content, SIRT3 immunofluorescence intensity, and GPX4, SLC7A11, and SIRT3 protein expression (P<0.05), with increased LDH activity, TfR1 protein expression, and MDA, Fe²⁺, and ROS levels (P<0.05). Compared with the model group, the GE group exhibited increased cell viability, GSH content, SIRT3 immunofluorescence intensity, and GPX4, SLC7A11, and SIRT3 protein expression (P<0.05), and decreased LDH activity, TfR1 protein expression, and MDA, Fe²⁺, and ROS levels (P<0.05). Compared with the GE group, the SIRT3 inhibitor group showed reduced cell viability, GSH content, SIRT3 immunofluorescence intensity, and GPX4, SLC7A11, and SIRT3 protein expression (P<0.05), along with elevated LDH activity, TfR1 protein expression, and MDA, Fe²⁺, and ROS levels (P<0.05). Conclusions Geniposide alleviates LPS-induced inflammatory injury in HCAECs, and the mechanism may involve inhibition of ferroptosis and activation of SIRT3 signaling.