摘要
目的 探讨银杏内酯 (Gin)对培养的皮层神经细胞的抗缺氧效应及其机制。方法 对原代培养的小鼠皮层神经细胞 ,进行随机分组 ,每个实验均分为正常对照组、缺氧组和 Gin组 ,每组做 8份重复测试。通过电镜观察神经细胞形态结构变化、利用甲基四唑蓝 (MTT)比色法检测细胞活性、速率法测定乳酸脱氢酶 (L DH)释放量、黄嘌呤氧化酶法检测超氧化物歧化酶 (SOD)活性、硫代巴比妥酸法测定丙二醛 (MDA )含量、硝酸还原酶比色法测定一氧化氮 (NO)含量 ,观察 Gin对缺氧神经细胞的影响。结果 (1)电镜观察显示 ,缺氧组神经细胞呈变性至坏死等不同程度的损伤 ;Gin组神经细胞细胞膜完整 ,微绒毛清晰可见 ,线粒体结构保存较好 ,与未缺氧的对照组相似。 (2 )缺氧后神经细胞活性 (0 .6 0 6±0 .0 35 )较正常对照组 (0 .6 77± 0 .0 2 8)降低 ,L DH释放量 (5 9.333± 9.5 2 1) U· ml- 1 · min- 1 较正常对照组 (38.5 0 0± 11.82 8) U· ml- 1 · min- 1 升高 ,其差异均有显著性意义 ;而预先给予 Gin的神经细胞活性(0 .6 4 5± 0 .0 2 7)明显高于缺氧组 ,L DH释放量 (40 .0 0 0± 6 .812 ) U· m l- 1 · m in- 1 显著低于缺氧组。 (3)缺氧后神经细胞 SOD活性 (46 .4 73± 7.4 72 ) NU / mg蛋白明显低于正常对照组 (5
Objective To explore the protective effects and the mechanism of Ginkgolides(Gin) on anoxic injury of cultured cortical neurons. Methods In every experiment, cultured mouse cortical neurons were divided randomly into three groups(control group,anoxia group and Gin group). All the groups underwent eight repeated neuron testing to observe the effects of Gin on anoxic neurons. Changes in the neuronal morphology were observed by electromicroscopy; neuronal viability was determined by MTT assay; MDA contents were measured by thiobarbituric acid method; SOD activity was determined by xanthine oxidase method and NO content was measured by nitrate reductase chromatometry. Results (1) With electromicroscopy, the neurons in the anoxia group were found injured, varying from degeneration to necrosis; however, the morphology of anoxic neurons with the pretreatment of Gin was similar to that in the un anoxia group: the damage was reduced obviously; the cytomembrane is integrate; the microvilli were claerly discernible; the mitochondrial structure was well preserved. (2) The neuronal viability was decreased, and the LDH release was increased after anoxia, compared with those in the control group; through the pretreatment with Gin, the neuronal viability was evidently higher and the LDH release was significantly lower than those in the anoxia group, respectively. (3) Compared with the control group, the SOD activity of neurons was decreased and the MDA content was increased due to anoxia; while the SOD activity and the MDA content in the Gin group became significantly higher and remarkably lower than those in the anoxia group, respectively. (4) The NO content in the neuronal cultured medium in the anoxia group was higher than that in the control group; the NO content of neurons in the Gin group was significantly lower than that in the anoxia group. Conclusions (1) Gin has affirmative protective effects on anoxia induced neuronal damage. (2) The anti anoxia effects of Gin may be related to its functions of enhancing the an
出处
《中华航海医学与高气压医学杂志》
CAS
CSCD
2002年第3期155-160,共6页
Chinese Journal of Nautical Medicine and Hyperbaric Medicine
基金
交通部重点科技项目 (95 0 40 3 41)
