【目的】　探讨一氧化氮在顺铂肾毒性氧化应激机制中的作用。【方法】　采用少量多次给大鼠腹腔注射顺铂 (CP)及经口给予水飞蓟素 (SB)预处理后给予CP模型 ,观察血尿素氮 (BUN)含量、一氧化氮 (NO)含量、一氧化氮合酶 (NOS)活性、丙二醛 (MDA)形成、超氧化物歧化酶 (SOD)活性等指标的变化。【结果】　CP可诱导NOS活性增高 ,使NO生成量增多 ;BUN含量与MDA含量及SOD活性的变化并不完全一致 ,而与NO含量的时相变化趋势基本一致 ;SB可使BUN含量、MDA含量及NO含量降至对照组水平 ,同时可使SOD活性明显升高。【结论】　NO可能在CP所致肾损害中起更重要的作用 ,SB可预防CP所致的肾损害 ,其机制可能与SB降低NO生成量、升高SOD活性有关 【Objective】 To investigate the role of nitric oxide in cisplatin nephrotoxicity-induced oxidative stress. 【Methods】 The CP model was induced by intraperitoneal injection of cisplatin (CP) and oral administration of silybin (SB) in a small amount for several times. The levels of blood urea nitrogen (BUN), nitric oxide (NO) NOS activity, malondialdehyde (MDA) formation and superoxide dismutase (SOD) activity. 【Result】 CP could induce the increase of NOS activity and increase the production of NO. The changes of BUN content and MDA content and SOD activity were not consistent with the changes of NO content, but the content of BUN, MDA Content and NO content decreased to the level of the control group, while SOD activity was significantly increased. 【Conclusion】 NO may play a more important role in CP-induced renal damage. SB may prevent CP-induced renal damage, which may be related to SB decreasing NO production and increasing SOD activity