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研究神经生长因子（ＮＧＦ）对一氧化氮（ＮＯ）介导的大鼠脑皮质神经无毒性的影响。方法：用原代培养的大鼠胎鼠脑皮质神经细胞，测定ＮＯ含量及原生型一氧化氮合酶（ｃＮＯＳ）基因表达，并研究ＮＧＦ对细胞缺氧／缺糖损伤的影响。结果：细胞缺氧／缺糖培养 ２４ ｈ后，细胞死亡率明显增高，ＮＯ大量释放。 ＮＧＦ １００ μｇ／Ｌ显著提高细胞生存力，降低ＮＯ释放，但其对硝普钠（ＳＮＰ）３００ μｍｏｌ／Ｌ引起的ＮＯ大量释放及细胞死亡率升高无明显影响。 ＮＧＦ５０、１００ μｇ／Ｌ显著降低细胞缺氧／缺糖引起的 ｃＮＯＳ ｍＲＮＡ的高表达。结论：ＮＯ介导了细胞缺氧／缺糖损伤，ＮＧＦ通过抑制ｃＮＯＳ活性，降低ＮＯ释放来保护神经元免受缺氧／缺糖损伤。
To investigate the effects of nerve growth factor (NGF) on nitric oxide (NO) -mediated neurotoxicity in rat cortical neurons. Methods: Primary cultured rat fetal rat cortical neurons were used to determine NO content and expression of cNOS gene. The effects of NGF on hypoxia / hypoglycemic injury were investigated. Results: After 24 h of hypoxia / glucose deprivation, cell death rate was significantly increased and NO was released in a large amount. NGF at 100 μg / L significantly increased cell viability and NO release, but had no significant effect on NO release caused by 300 μmol / L sodium nitroprusside (SNP) and increased cell death rate. NGF50 and 100 μg / L significantly decreased the expression of cNOS mRNA induced by hypoxia / glucose deprivation. CONCLUSION: NO mediates cell hypoxia / glucose deprivation, and NGF protects neurons from hypoxia / glucose deprivation by inhibiting cNOS activity and decreasing NO release.