摘要
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。
Purpose: Effects of nerve growth factor (NGF) on nitric oxide(NO)-mediated neurotoxicity in cultured neurons of cerebral cortex were studied. Methods: NO release and constitutive nitric oxide synthase (cNOS) mRNA level were measured in cultures of cerebral cortex from fetal rats, and the effects of NGF on NO-mediated neurotoxicity were studied. Results: There was a marked increase of neuronal death and NO release in oxygen/ glucose deprived cultures for 24 h. NGF 50, 100 μg/L significantly increased neuronal surviving and decreased NO release. However, it had no significantly effects on neurotoxicity induced by sodium nitroprusside (SNP) 300 umol/L in conical cultures. NGF significanlty attenuated cNOS gene expression. Conclusion: NO mediates the neurotoxicity of hypoxia/ hypoglycemia and NGF protects conical neurons against oxygen/glucose deprivation induced toxicity via inhibiting the activity of cNOS and the release of NO.
出处
《中国生化药物杂志》
CAS
CSCD
1999年第4期170-173,共4页
Chinese Journal of Biochemical Pharmaceutics
关键词
脑缺血
神经生长因子
一氧化氮
神经元
大鼠
Nerve growth factor, Nitric oxide, Nitric oxide synthase, Hypoxia, Neurons