目的 动态观测大肠杆菌内毒素(LPS)诱导新生大鼠肝损伤时NO，SOD，MDA的变化及地塞米松(Dex)对肝脏的保护作用。方法 取7日龄新生Wistar大鼠120只，分为正常对照组(A)、内毒素组(B)和地塞米松组(C)。B组为腹腔注射LPS 5 mg/kg制成内毒素血症模型，C组为LPS 5 mg/kg+Dex 5 mg/kg共同腹腔注射，A组用等体积生理盐水腹腔注射。观测3组新生鼠2 h，4 h，6 h，24 h时肝组织匀浆NO，SOD，MDA改变，同时对肝脏结构行光镜和电镜检查。结果 ①与A组相比，B组LPS作用后随时间延长引起SOD下降，其中24 h降至最低值［(118.96±12.81) NU/mg.pro］(P<0.01)；而NO，MDA升高，6 h NO达最高值［(2.58±0.31) μmol/g.pro］(P<0.01)，4 h MDA达最高值［(2.61±0.50) nmol/mg.pro］(P<0.05)。C组应用Dex处理后4 h和6 h SOD明显上升，而NO与MDA明显下降，与B组比较，差异有显著性(P<0.05或0.01)。②B组光镜下可见肝组织大量炎性细胞浸润，肝细胞点状坏死及出血；电镜下可见线粒体嵴明显减少，内质网扩张，出现凋亡小体及核固缩。C组上述病理变化明显减轻。结论 LPS诱导新生大鼠肝损伤，肝组织匀浆NO和MDA含量明显上升，SOD活性明显下降；Dex对急性肝损伤有保护作用，可能与抑制NO的过量产生及清除氧自由基有关。

OBJECTIVE: To observe the dynamic changes of nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA) and the protective effect of dexamethasone (Dex) on the liver when Lipopolysaccharide (LPS) induces hepatic injuries in neonatal rats. METHODS: One hundred and twenty seven day neonatal rats were divided into the control group (Group A), LPS group (Group B), and Dex group (Group C). Group B rats received 5 mg/kg LPS intraparitoneally. Group C was given LPS 5 mg/kg+Dex 5 mg/kg, and Group A was injected with normal saline of the same volume. NO and MDA contents and SOD activity were detected by the biochemical method in the liver tissues at different times. At the same time, the structural changes of the liver were observed under the light microscope and electron microscope. RESULTS: ① NO and MDA contents increased in Group B compared with Group A. NO content reached its maximum [( 2.58 ± 0.31 ) μmol/g.pro] at 6 h after LPS was given (P< 0.01 ); MDA content reached its maximum ( 2.61 ± 0.50 ) nmol/mg.pro] at 4 h after LPS was given (P< 0.05 ). SOD activity in Group B decreased as time was increasing compared with Group A. It dropped to its minimum [( 118.96 ± 12.81 ) NU/mg.pro] at 24 h (P< 0.01 ). NO and MDA contents decreased significantly and SOD activity increased significantly at 4 h and 6 h in Group C compared with Group B (P< 0.05 or 0.01 ). ② In group B, a large amount of inflammatory cell infiltration in liver tissues were noted and hepatic cells showed spotty necrosis and bleeding under the light microscope; the electron microscope showed a significant decrease of mitochondria cristae, the broadness of endoplasmic reticula, hepatic cell necrosis and karyopyknosis. The structural changes were alleviated in Group C. CONCLUSIONS: LPS could cause changes of NO and MDA contents and SOD activity in hepatic tissues. Dex might inhibit NO production and get rid of oxygen free radicals so that it can protect the liver from injuries.