神经节苷脂GM_1对新生鼠缺血缺氧后NOS表达的影响  

Expressions of nitric oxide synthase in neonatal rat after hypoxia-ischemia and their changes while ganglioside GM_1 administrated

作　　者：胡志兵[1] 陆雪芬[2] 郑德枢[2] 邓平[2] 李婉媚[1] 

机构地区：[1]广州市第十二人民医院神经内科,广州510620 [2]广州医学院神经科学研究所,广州510180

出　　处：《中国临床药理学与治疗学》2002年第2期115-118,共4页Chinese Journal of Clinical Pharmacology and Therapeutics

基　　金：广东省医学科研基金资助项目 (№B2 0 0 110 1)

摘　　要：目的 :探讨神经节苷脂GM1对新生儿缺氧缺血性脑病的保护作用及可能机理。方法 :通过建立新生鼠缺氧缺血性脑病动物模型 ,观察缺血缺氧后不同时期脑组织的病理变化和一氧化氮合酶 (NOS)表达 ,以及GM1对其影响。结果 :GM1给药组脑组织损伤明显减轻 ,缺血缺氧可诱导脑组织中NOS表达水平上调 ,GM1部分地抑制了缺血缺氧后NOS的表达水平。结论 :GM1对新生儿缺氧缺血性脑损伤具有一定程度的保护作用 ,其作用可能是通过部分抑制NOS的表达。AIM: To study the neuroprotective effect and possible mechanism of ganglioside GM 1 on neonatal hypoxic-ischemic-encephalopathy(HIE). METHODS: A rat model of neonatal HIE was established, then the pathological changes and expressions of nitric oxide synthase (NOS) in the brain tissues were investigated in different periods after hypoxia-ischemia (HI) and the subseqent changes of the above results after GM 1 administrated. RESULTS: The damage of the brain exposed to HI were alleviated significantly after GM 1 administrated. The levels of NOS expressions in the brain tissue increased after HI. GM 1 could inhibit NOS expressions induced by HI. CONCLUSION: GM 1 may have some protective effects on neonatal HIE, and the possible mechanism is related to the partial inhibition of NOS expression.

关 键 词：神经节苷脂GM1 缺氧缺血性脑病 新生鼠 一氧化氮合酶 

分 类 号：R965[医药卫生—药理学] R748[医药卫生—药学]