目的：探讨萝卜硫素对N-硝基-L-精氨酸甲酯（L-NAME）诱导的人胎盘滋养细胞氧化应激和凋亡的影响及其可能机制。方法：人胎盘滋养细胞株HTR-8/SV-neo用不同浓度（10、20、40 μmol·L^-1）萝卜硫素培养72 h，或用15 μmol·L^-1 c-Jun氨基末端激酶/p38丝裂原活化蛋白激酶（JNK/p38 MAPK）信号通路阻断剂SB203580培养24 h，再用100 μmol·L^-1 L-NAME干预48 h。细胞计数试剂盒-8（CCK-8）和Annexin V-FITC/PI检测细胞存活率与凋亡率，硫代巴比妥酸比色法检测丙二醛（MDA）含量，化学比色法检测超氧化物歧化酶（SOD）、谷胱甘肽（GSH）活性，酶联免疫吸附测定（ELISA）法检测细胞中肿瘤坏死因子-α（TNF-α）、白细胞介素（IL）-1β、IL-6含量，原位缺口末端标记法（TUNEL）染色检测细胞凋亡，蛋白质印迹法检测JNK/p38 MAPK信号通路相关蛋白表达。结果：与模型组比较，在10、20、40 μmol·L^-1萝卜硫素和15 μmol·L^-1 SB203580作用下，细胞存活率增加（P<0.05），细胞凋亡率下降（P<0.05），TUNEL染色细胞数目减少（P<0.05），细胞中MDA含量减少而SOD、GSH活性均升高（P<0.05），TNF-α、IL-1β和IL-6含量减少（P<0.05）；同时在20、40 μmol·L^-1萝卜硫素和15 μmol·L^-1 SB203580作用下，细胞中p-JNK和p-p38MAPK的蛋白表达均降低（P<0.05）。结论：萝卜硫素能够改善L-NAME诱导的胎盘滋养细胞的氧化应激反应，减轻炎症反应并抑制细胞凋亡，其作用机制可能与抑制JNK/p38 MAPK信号通路激活有关。

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