目的 探究枸橼酸咖啡因治疗早产儿支气管肺发育不良（BPD）的作用及分子机制。方法 构建新生大鼠和MLE-12肺上皮细胞的高氧BPD模型，分别设立对照组、高氧组和低、中、高剂量枸橼酸咖啡因干预组。运用H&E染色、免疫荧光染色、CCK8细胞凋亡实验、流式细胞凋亡检测等技术评估枸橼酸咖啡因的作用。进一步通过活性氧（ROS）免疫荧光检测、电镜观察、蛋白质免疫印迹等检测线粒体应激及细胞凋亡的发生情况。结果 枸橼酸咖啡因干预可提高高氧暴露后新生大鼠的生存率，促进体重增长，改善肺组织损伤；枸橼酸咖啡因干预提高了MLE-12细胞的存活率，减少表面活性蛋白C（SPC）的丢失并抑制细胞凋亡。机制上，枸橼酸咖啡因可降低ROS水平，修复线粒体结构，调节线粒体应激通路（eIF2α-ATF4-CHOP）和线粒体凋亡途径相关蛋白（Bax、Bcl2、Cleaved caspase-3）的表达。结论 枸橼酸咖啡因通过减轻线粒体氧化应激，抑制细胞凋亡，改善高氧诱导的肺损伤，在早产儿BPD治疗中发挥积极作用。

Objective To explore the role and mechanism of caffeine citrate in the treatment of bronchopulmonary dysplasia (BPD) in premature infants. Methods Hyperoxic BPD models of neonatal rats and MLE-12 lung epithelial cells were constructed, and the control group, hyperoxic group, and low, medium, and high dose of caffeine citrate intervention groups were set up respectively. The effects of caffeine citrate were evaluated using H&E staining, immunofluorescence staining, CCK8 apoptosis assay, and flow cytometry apoptosis detection. The occurrence of mitochondrial stress and apoptosis was further detected by reactive oxygen species (ROS) immunofluorescence assay, electron microscopy observation, and western blot assay. Results Caffeine citrate intervention increased the survival rate, promoted the body weight gain, and ameliorated the lung tissue injury in neonatal rats after hyperoxia exposure. Caffeine citrate intervention increased the survival rate of MLE-12 cells, reduced the loss of surfactant protein C (SPC), and inhibited apoptosis. In terms of mechanism of action, caffeine citrate reduced the level of reactive oxygen species (ROS), repaired mitochondrial structure, and regulated the expression of proteins related to mitochondrial stress pathways (eIF2α-ATF4-CHOP) and mitochondrial apoptotic pathways (Bax, Bcl2 and Cleaved caspase-3). Conclusions Caffeine citrate ameliorates hyperoxia-induced lung injury by repairing mitochondrial function and inhibiting oxidative stress and apoptosis, which plays an active role in the treatment of BPD in preterm infants.