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作 者:邢玉凤 刘东海 张淑红[1] 张玉萍[1] 朱金玲[1]
机构地区:[1]佳木斯大学基础医学院,黑龙江佳木斯154007
出 处:《中风与神经疾病杂志》2017年第10期924-926,共3页Journal of Apoplexy and Nervous Diseases
基 金:佳木斯大学创新团队项目资助(No.CXTDPY-201602)
摘 要:目的探讨阿魏酸(Ferulic acid,FA)对戊四氮致癫痫大鼠海马组织中Bax和Bcl-2蛋白表达的影响,近而讨论FA对戊四氮致癫痫鼠海马神经元的保护作用。方法将60只雄性健康的Wister大鼠随机分为生理盐水组、模型组(PTZ 35 mg/kg)和阿魏酸干预组(50 mg/kg),均采用腹腔注射的方式,连续注射28 d,停止给药1 d后处死实验大鼠、取材。应用免疫组织化学技术和Western blot方法来检测Bax和Bcl-2的表达情况,用来判断癫痫所导致的细胞凋亡情况。结果阿魏酸干预组大鼠的海马组织Bax的表达量明显低于模型组,差异有显著性(P<0.01),Bcl-2的表达量高于模型组,差异有显著性(P<0.01);生理盐水组大鼠的海马组织内Bax的表达量明显低于模型组,差异有显著性(P<0.01),Bcl-2表达量明显高于模型组,差异有显著性(P<0.01)。结论阿魏酸对戊四氮致癫痫大鼠海马神经元损伤具有保护作用,其保护作用机制可能与其抑制鼠脑细胞凋亡有关。Objective To investigate the effect of ferulic acid(FA) on the expression of Bax and Bcl-2 protein in hippocampus of pentylenetetrazole(PTZ)-induced epilepsy rats,and to discuss the protective effect of FA on hippocampal neurons in pentylenetetrazol-induced epilepsy effect.Methods 60 male healthy wister rats were randomly divided into saline group,model group(PTZ 35 mg/kg) and ferulic acid intervention group(50 mg/kg).The rats were injected intraperitoneally with continuous28 days,the rats were sacrificed after one day.Immunohistochemistry and Western blot were used to detect the expression of Bax and Bcl-2,which were used to determine the apoptosis induced by epilepsy.Results The expression of Bax in the hippocampus was significantly lower than that in the model group(P〈0.01).The expression of Bcl-2 was significantly higher than that of the model group(P〈0.01).Conclusion Ferulic acid has protective effect on hippocampal neuronal injury induced by pentylenetetrazole in epilepsy rats,and its protective mechanism may be related to its inhibition of brain cell apoptosis.
分 类 号:R742.1[医药卫生—神经病学与精神病学]
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