目的 观察人参皂苷 Rb1（ginsenoside Rb1，G⁃Rb1）对高氧诱导新生仔鼠肺损伤的改善作用 及相关机制。方法 模型组、Rb1 组、Rb1 联合 ML385 组建立新生仔鼠高氧肺损伤模型。Rb1 联合 ML385 组腹腔注射 G⁃Rb1（10 mg/kg）+灌胃 ML385（20 mg/kg），Rb1 组腹腔注射 G⁃Rb1（10 mg/kg）+灌胃等量生理盐水，空白组、模型组腹腔注射、灌胃等量生理盐水。检测丙二醛（malondialdehyde，MDA）、超氧化物歧化酶 （superoxide dismutase，SOD）活性；检测肺表面活性物质蛋白⁃D（alveolar surface active substance⁃D，SP⁃D）含 量；检测肺组织核因子 E2 相关因子 2（nuclear factor⁃E2 related factor2，Nrf2）蛋白表达量。结果 与模型组 比较，Rb1 组 MDA 水平、SP⁃D 水平降低，SOD 活性、Nrf2 蛋白表达量升高（P < 0.05）；与 Rb1 组比较，Rb1 联 合 ML385 组 MDA 水平、SP⁃D 水平升高，SOD 活性、Nrf2 蛋白表达量降低（P < 0.05）。结论 G⁃Rb1 可改善新生仔鼠肺损伤，提升机体抗氧化能力，抑制肺组织氧化应激反应，激活 Nrf2/ARE 通路可能是其发挥作用的机制之一。

Objective To observe the improvement effect of ginsenoside Rb1（G⁃Rb1）on lung injury of neonatal rats induced by hyperoxia，and to explore its mechanism. Method Hyperoxic lung injury model of neonatal rats was established in model group，Rb1 group，and Rb1 combined with ML385 group. Rb1 combined with ML385 group was intraperitoneally injected with G⁃Rb1（10 mg/kg）+ intragastric ML385（20 mg/kg）；Rb1 group with G⁃Rb1 （10 mg/kg）+ gavage the same amount of normal saline and the blank group and model group with the same amount of normal saline + gavage with the same amount of normal saline. The activity of malondialdehyde（MDA）and superoxide dismutase（SOD），the content of lung surface active substance protein⁃D（SP⁃D）and the expression of Nrf2 protein in lung tissue were detected. Results Compared with those in model group，MDA level and SP⁃D level in Rb1 group were decreased，but SOD activity and Nrf2 protein expression were increased（P < 0.05）. Compared with those in Rb1 group，MDA level，and SP ⁃D level in Rb1 combined with ML385 group were increased，but SOD activity，and Nrf2 protein expression were decreased（P < 0.05）. Conclusion G⁃Rb1 can improve lung injury of newborn mice，enhance the body′s antioxidant capacity，and inhibit the oxidative stress response of lung tissue. Activation of the Nrf2/ARE pathway may be one of its mechanisms.