高氧致新生鼠肺损伤时肾组织一氧化氮及氧自由基的变化

Changes of nitric oxide and oxygen free radical in the kidney of neonatal rats with prolonged hyperoxic lung injury

摘要:

目的 观察持续吸入高氧致新生大鼠肺损伤时肾组织自由基的变化,以探讨高氧对肾脏的损伤。 方法 采用高氧致新生鼠肺损伤的模型,将足月新生鼠生后分别在90%±5%氧气(n=140)和正常空气(n=88) 中持续暴露,于1,3,7,14,21d各处死8只,用分光光度计比色法动态测定肺和肾组织中超氧化物歧化酶(SOD)活 性、丙二醛(MDA)和一氧化氮(NO)含量的变化。结果 高氧暴露3d肺组织SOD的活性开始增高,7d时明显高 于对照组(214±19KNU/gvs186±19KNU/g,P<0.01),并逐渐增高持续至14d(220±15KNU/gvs197±21 KNU/g,P<0.05)和21d(251±15KNU/gvs195±8KNU/g,P<0.01);MDA含量于高氧暴露3d开始增高并高 于对照组(28.1±2.0μmol/gvs21.1±1.3μmol/g,P<0.05),7d最高(30.8±4.2μmol/gvs19.9±2.2μmol/g, P<0.01),14d虽有下降但仍高于对照组(26.3±3.8μmol/gvs22.6±2.3μmol/g,P<0.05);NO水平则于7d 时有所增高并高于对照组(99±8μmol/gvs89±8μmol/g,P<0.05),14d(128±34μmol/gvs93±17μmol/g,P <0.05)和21d(171±34μmol/gvs106±25μmol/g,P<0.01)仍高于对照组。而高氧组肾组织SOD活性的改变 与对照比较无差异,MDA和NO含量改变较肺晚,于吸高氧14d时高于对照(分别为24.1±5.0μmol/gvs16.0± 1.9

Abstract:

Objective To examine the changes of nitric oxide and oxygen free radical in the kidneys of neonatal rats with lung injury induced by prolonged hyperoxia in order to study the induction of renal damage by prolonged hyperoxic exposure. Methods Full-term newborn rats were continuously exposed to oxygen (90%±5% O 2,n=140) or room air (21% O 2,n=88) after birth. Dynamic changes of superoxide dismutase (SOD) activity and content of malondialdehyde (MDA) and nitric oxide (NO) in the lung and kidney were monitered by spectrophotometer on days 1, 3, 7, 14 and 21 in the Hyperoxia and Control group. Results In the Hyperoxia group, SOD activity in lungs began to increase on the 3rd day, and significantly higher than that of controls on the 7th day (214±19 KNU/g vs 186±19 KNU/g, P< 0.01), 14th day (220±15 KNU/g vs 197±21 KNU/g, P< 0.05) and 21th day (251±15 KNU/g vs 195±8 KNU/g, P< 0.01). The MDA level in the lungs increased on the 3rd day ( 28.1± 2.0 μmol/g vs 21.1± 1.3 μmol/g, P< 0.05) and reached a peak on the 7th day ( 30.8± 4.2 μmol/g vs 19.9± 2.2 μmol/g, P< 0.01), then decreased but still remained higher than controls on the 14th day ( 26.3± 3.8 μmol/g vs 22.6± 2.3 μmol/g, P< 0.05). The NO level began to increase and was higher than controls on the 7th day (99±8 μmol/g vs 89±8 μmol/g, P< 0.05), and 14th day (128±34 μmol/g vs 93±17 μmol/g, P< 0.05) and 21st day (171±34 μmol/g vs 106±25 μmol/g, P< 0.01). In the kidney, although there was little difference in SOD activities between two groups, the levels of MDA and NO increased on the 14th day ( 24.1± 5.0 μmol/g vs 16.0± 1.9 μmol/g, P< 0.01; 286±71 μmol/g vs 222±45 μmol/g, P< 0.05), continuously to 21st day ( 16.5± 2.2 μmol/g vs 13.0± 2.7 μmol/g, P< 0.05; 298±65 μmol/g vs 204±49 μmol/g, P< 0.01). These changes appeared later than in the lungs. Conclusions Renal damage can be induced by prolonged hyperoxia exposure and be developed behind lung injury in neonatal rats.