目的 探讨成纤维细胞生长因子（fibroblast growth factor, FGF）19在高糖（high glucose, HG）导致的血管内皮细胞炎症损伤中的作用及其机制。 方法 将人脐静脉内皮细胞（human umbilical vein endothelial cell, HUVEC）随机分为对照组、HG组、FGF19组、HG+FGF19组（n=3）。运用CCK8法检测不同浓度葡萄糖和/或FGF19对HUVEC细胞活力的影响，流式细胞术检测FGF19对HUVEC细胞凋亡的影响，ELISA法测定白细胞介素-6（interleukin 6, IL-6）、诱导型一氧化氮合酶（inducible nitric oxide synthase, iNOS）、总超氧化物歧化酶（total superoxide dismutase, T-SOD）、丙二醛（malondialdehyde, MDA）水平，实时荧光定量PCR及Western blot法检测血管内皮生长因子（vascular endothelial growth factor, VEGF）、红系衍生的核因子2相关因子2（nuclear factor erythroid 2 related factor 2, Nrf2）、血红素加氧酶-1（heme oxygenase-1, HO-1）mRNA及蛋白表达水平；另取细胞分为对照组、siRNA-Nrf2（siNrf2）组、HG组、HG+FGF19组、HG+FGF19+阴性对照组、HG+FGF19+siNrf2组（n=3），观察沉默Nrf2基因后FGF19对HG诱导的HUVEC氧化应激损伤的影响。 结果 与对照组比较，HG组细胞凋亡率和IL-6、iNOS、MDA含量以及VEGF mRNA及蛋白表达升高（P<0.05），T-SOD活力以及Nrf2、HO-1 mRNA及蛋白表达降低（P<0.05）；与HG组比较，HG+FGF19组细胞凋亡率和IL-6、iNOS、MDA含量以及VEGF mRNA及蛋白表达降低（P<0.05），T-SOD活力以及Nrf2、HO-1 mRNA及蛋白表达水平升高（P<0.05）。与HG+FGF19+阴性对照组相比，HG+FGF19+siNrf2组T-SOD活力下降，MDA含量升高（P<0.05）。 结论 FGF19可减轻HG导致的血管内皮细胞炎症损伤，其机制可能与Nrf2/HO-1信号通路有关。

Objective To investigate the role and mechanism of fibroblast growth factor (FGF) 19 in inflammation-induced injury of vascular endothelial cells caused by high glucose (HG). Methods Human umbilical vein endothelial cells (HUVECs) were randomly divided into four groups: control, HG, FGF19, and HG+FGF19 (n=3 each). The effect of different concentrations of glucose and/or FGF19 on HUVEC viability was assessed using the CCK8 assay. Flow cytometry was utilized to examine the impact of FGF19 on HUVEC apoptosis. Levels of interleukin-6 (IL-6), inducible nitric oxide synthase (iNOS), total superoxide dismutase (T-SOD), and malondialdehyde (MDA) were measured by ELISA. Real-time quantitative PCR and Western blotting were used to determine the mRNA and protein expression levels of vascular endothelial growth factor (VEGF), nuclear factor erythroid 2 related factor 2 (Nrf2), and heme oxygenase-1 (HO-1). Cells were further divided into control, siRNA-Nrf2 (siNrf2), HG, HG+FGF19, HG+FGF19+negative control, and HG+FGF19+siNrf2 groups (n=3 each) to observe the effect of FGF19 on oxidative stress injury in HUVECs induced by high glucose after silencing the Nrf2 gene. Results Compared to the control group, the HG group exhibited increased apoptosis rate, increased IL-6, iNOS and MDA levels, and increased VEGF mRNA and protein expression, along with decreased T-SOD activity and decreased mRNA and protein expression of Nrf2 and HO-1 (P<0.05). Compared to the HG group, the HG+FGF19 group showed reduced apoptosis rate, decreased IL-6, iNOS and MDA levels, and decreased VEGF mRNA and protein expression, with increased T-SOD activity and increased Nrf2 and HO-1 mRNA and protein expression (P<0.05). Compared to the HG+FGF19+negative control group, the HG+FGF19+siNrf2 group had decreased T-SOD activity and increased MDA levels (P<0.05). Conclusions FGF19 can alleviate inflammation-induced injury in vascular endothelial cells caused by HG, potentially through the Nrf2/HO-1 signaling pathway.