摘要
目的 :探讨银杏内酯 (ginkgolides ,Gin)对过氧化氢 (H2 O2 )诱导的皮层神经细胞损伤的保护作用及其机制。方法 :在小鼠皮层神经细胞的培养基中加入H2 O2 ,建立神经细胞氧化损伤模型 ,利用MTT比色法检测细胞存活率 ,Westernblot技术分析c fos、c jun基因表达产物C FOS蛋白、C JUN蛋白的变化。结果 :H2 O2 可诱导原代培养的神经细胞损伤和存活率降低 ,其损伤作用呈现浓度和时间依赖性 ;同时可诱导神经元C FOS、C JUN表达增加。Gin预处理2 4h可明显减轻神经细胞形态学改变 ,提高神经细胞存活率 ,且在 0～ 37.5mg·L-1范围内呈现浓度依赖关系。Gin能明显逆转H2 O2 诱导的C JUN蛋白表达的增高 ,对H2 O2 刺激的C FOS蛋白表达无明显影响。结论 :Gin可对抗H2 O2 引起的神经细胞损伤 ,该保护作用与其抑制细胞c jun基因过度表达有关。
AIM: To observe the protective effect and mechanism of ginkgolides (Gin) on H_2O_2-induced neurocytes injury. METHODS: H_2O_2 was added to the medium of mouse cortical neurons in order to establish H_2O_2-injured model. Neurocytes survival rate was determined by MTT assay, and the expression of c-fos and c-jun genes was analyzed with Western blot. RESULTS: There was reverse concentration-time-relationship between the treatment of H_2O_2 and neurocytes survival rate, while the expression levels of c-fos and c-jun of neurons increased significantly after treatment of H_2O_2. The pretreatment of Gin for 24 h could relieve the morphologic damage of neurons and enhance the neurocytes survival rate. The protective effect of Gin was increased in the range from 0 to 37.5 mg·L -1 . Furthermore, Gin could inverse the C-JUN expression of neurons induced by H_2O_2, but had no obvious effects on C-FOS. CONCLUSION: Gin protects neurons from H_2O_2-injury via inhibiting over-expression of the c-jun genes.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2003年第4期401-404,共4页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
交通部重点科技项目 (№ 95 0 40 3 41)
