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目的 探讨神经元型一氧化氮合酶 (nNOS)及其选择性抑制剂 7 硝基吲唑 (7 NI)在新生大鼠缺氧缺血性脑损伤 (HIBD)中的作用。方法 制备新生大鼠HIBD模型 ,用RT PCR的方法测定HIBD组缺氧开始后 0h、1h、2h、6hnNOSmRNA的表达 ,同对照组相应时点比较。测定HIBD组、7 NI组缺氧开始后 1h、2h、6h、8h以及对照组一氧化氮合酶 (NOS)、一氧化氮 (NO)、丙二醛(MDA)、超氧化物歧化酶 (SOD)的含量并作相应比较 ,另用TUNEL法比较 3组缺氧结束后 2 4h神经细胞凋亡的情况。结果 在缺氧开始后 2h和 6hHIBD组nNOSmRNA表达高于对照组 (P <0 0 5 ) ,且以 6h表达更高 (P <0 0 5 )。HIBD组各时点与对照组比较NOS、NO、MDA值升高 (P <0 0 1) ,SOD值下降 (P <0 0 1) ,而 7 NI组各时点MDA、NOS和NO值较HIBD组下降 (P <0 0 5 ) ,SOD值升高 (P <0 0 5 ) ,1h时点测定值接近对照组水平。对照组未见明显细胞凋亡情况 ,7 NI组比HIBD组凋亡减少 ,差异具有显著性 (P <0 0 0 1)。结论 nNOS参与了新生鼠HIBD的形成 ,其抑制剂 7 NI通过抗氧化和抑制凋亡发挥了神经保护作用。
Objective To investigate the role of nitric oxide synthase (nNOS) and its selective inhibitor 7 nitroindazole (7 NI) in neonatal rats with hypoxic-ischemic brain damage (HIBD). Methods HIBD model was established in neonatal rats. RT-PCR was used to detect the expression of 6hNNOS mRNA at 0h, 1h, 2h and 6h after hypoxia in HIBD group, compared with the control group. The levels of nitric oxide synthase (NOS), nitric oxide (NO), malondialdehyde (MDA), superoxide dismutase (SOD) and malondialdehyde (MDA) in the NIH group were measured at 1, 2, 6, SOD) were compared and the corresponding TUNEL method was used to compare the neuronal apoptosis at 24 hours after the end of hypoxia. Results The expression of nNOS mRNA in HIBD group was higher than that in control group at 2h and 6h after hypoxia (P <0.05), and was higher at 6h (P <0.05). Compared with control group, the levels of NOS, NO and MDA in HIBD group increased (P <0.01) and SOD decreased (P <0.01), while the levels of MDA, NOS and NO in 7 NI group were significantly higher than those in control group HIBD group decreased (P <0 05), SOD value increased (P <0 05), and the measured value at 1 hour was close to that of control group. There was no obvious cell apoptosis in the control group. The apoptosis in 7 NI group was lower than that in HIBD group, the difference was significant (P <0.01). Conclusions nNOS is involved in the formation of HIBD in neonatal rats, and its inhibitor 7 NI exerts neuroprotective effect through anti-oxidation and apoptosis inhibition.