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目的 探讨新生大鼠缺氧缺血后脑内诱生型一氧化氮合酶 (i NOS)基因表达的变化及地塞米松 (DEX)对其的调控作用 ,从而阐明 DEX预处理对缺氧缺血新生动物神经保护作用的可能机制。 方法 建立新生儿缺氧缺血性脑病 (HIE)标准化的动物模型 ,应用快速竞争性逆转录 PCR技术 ,分别对缺氧缺血、DEX预处理后予缺氧缺血、缺氧缺血后即刻予 DEX、DEX加假手术及正常对照 5组新生大鼠的实验 ,对大脑组织中 i NOS m RNA的表达进行半定量分析。 结果 新生大鼠缺氧缺血后 ,缺血侧大脑 i NOS m RNA表达自 6 h开始 ,2 4h达高峰 ,7d时回至基线水平。DEX预处理可以抑制缺血侧大脑 i NOS m RNA的表达 ,而缺氧缺血后即刻注射 DEX对 i NOS m RNA的表达无明显调节作用。 结论 一氧化氮的产生可能在缺氧缺血后脑组织损伤的演变过程中起着重要的病理作用 ,EDX预处理对中枢神经的保护作用部分可能是通过抑制 i NOS m RNA的表达来实现的。
Objective To investigate the changes of inducible nitric oxide synthase (iNOS) gene expression in neonatal rats after hypoxia-ischemia and the regulatory effect of dexamethasone (DEX) on them, so as to clarify the effect of DEX preconditioning on hypoxic-ischemic Possible mechanisms of neuroprotection in newborn animals. Methods The normal animal model of neonatal hypoxic-ischemic encephalopathy (HIE) was established. The rapid competitive reverse transcription-PCR was used to detect the hypoxic-ischemic, hypoxic-ischemic and post-hypoxic- To DEX, DEX plus sham operation and normal control group of 5 neonatal rats experiments, the expression of i NOS m RNA in brain tissue semi-quantitative analysis. Results After hypoxic-ischemic brain damage, the expression of iNOS m RNA in the ischemic brain began to peak at 6 h, peaked at 24 h and returned to baseline at 7 d. DEX pretreatment can inhibit the expression of iNOS m RNA in ischemic brain, while injecting DEX immediately after hypoxic-ischemic ischemia had no effect on the expression of iNOS m RNA. Conclusion The production of nitric oxide may play an important role in the development of brain injury after hypoxic-ischemic injury. The protective effect of EDX preconditioning on the central nervous system may be partly through inhibiting the expression of i-NOS m RNA.