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机构地区:[1]中南大学湘雅医院儿科
出 处:《中国中西医结合杂志》2004年第4期339-342,共4页Chinese Journal of Integrated Traditional and Western Medicine
基 金:国家自然科学基金资助 (No.39870 2 51 )
摘 要:目的探索过氧化氢 (H2 O2 )致星形胶质细胞损伤的实验条件 ,研究黄芩甙对大鼠神经元和星形胶质细胞氧应激损伤的保护作用。方法体外培养大鼠前脑星形胶质细胞和神经元 ,分别应用H2 O2 、黄芩甙及两者联用处理 ,应用MTT分析法测定细胞活力或存活率。结果不同浓度H2 O2 对星形胶质细胞存活率的影响各组间差异有显著性 (F =2 8 5 6 9,P <0 0 1)。同一浓度的H2 O2 对不同接种密度细胞的损伤程度不同 (F =5 4 39,P <0 0 1)。在 2 5~ 4 0 μmol/L浓度范围内 ,黄芩甙不影响各组神经元和星形胶质细胞的存活率 (神经元 ,F =0 4 9,P >0 0 5 ;星形胶质细胞 ,F =1 0 0 1,P >0 0 5 )。但黄芩甙对H2 O2 所致神经元和星形胶质细胞氧应激损伤有拮抗作用 (神经元 ,F =2 4 384 ,P <0 0 1;星形胶质细胞 ,F =5 0 0 0 ,P <0 0 1) ,黄芩甙浓度越高 ,则细胞存活率越高。结论构建了一个H2 O2 氧化损伤星形胶质细胞的模型。在 2 5~4 0 μmol/L浓度范围内 ,黄芩甙对神经元和星形胶质细胞均无毒性作用。但黄芩甙能够拮抗H2 O2 所致的神经元和星形胶质细胞氧化损伤 ,而且这种作用呈剂量依赖性。ObjectiveTo explore the experimental conditions for H_2O_2 to injure astrocytes and the effect of baicalin in protecting neuro ns and astrocytes from oxidative stress injury. MethodsNeurons and astrocytes from forebrain of rats we re cultured in vitro and treated with H_2O_2,baicalin and combination of the two,respectively. The cell viability or survival rate was determined using MTT. ResultsEffects of H_2O_2 in different concentrations o n survival rate of astrocytes showed significant difference (F= 28.569, P<0.01) in a dose-dependent manner. Degrees of H_2O_2 injury,wit h the same concentration of H_2O_2,on cells with different seeding density we re also significantly different (F=5.439,P<0 .01),and dose -dependently. Baicalin didn't influence the survival rate of neurons and astroc ytes when the concentration was within 2.5~40 μmol/L (for neurons,F =0.49, P>0.05;for astrocytes,F=1.001,P >0.05),but baicalin showed significant antagonism to the injury of oxidative stress (for n eurons,F=24.384,P<0.01;for astrocytes, F=5.000, P<0.01). The higher the concentration of bainalin,the higher the cell survival rate. ConclusionA model of astrocytes oxidative injury induce d by H_2O_2 is established. Baicalin shows no toxicity on neurons and astrocyt es when the concentration is within 2.5~40 μmol/L,but could antagonize the H _2O_2 caused oxidative injury on cells in a dose-dependent manner.
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