对羟基苯甲醛对神经元缺氧所致钙超载的抑制作用  

Inhibition Effect of 4-Hydroxybenzaldehydeon Calcium Channels in Neurons

作　　者：周晓楠[1] 宋雪兰[1] 柳弯 解宇环[1] 宋波[1] 何芳雁[1] 

机构地区：[1]云南中医学院基础医学院,昆明650500

出　　处：《天然产物研究与开发》2017年第8期1296-1301,共6页Natural Product Research and Development

基　　金：国家自然科学基金(81560664;81660677);云南省应用基础研究项目(2015FB205(-027))

摘　　要：通过复制大鼠原代皮层神经元缺糖缺氧/复糖复氧(OGD/Rep)损伤模型,采用MTT法检测细胞存活率、硝酸还原酶法检测NO释放量、流式细胞仪检测胞内钙离子浓度、Western Blot法及RT-PCR法检测神经元L型钙通道、NMDA型钙通道、TRPM7通道蛋白和基因的表达,评价天麻成分对羟基苯甲醛对OGD/Rep损伤致大鼠原代皮层神经元钙通道过度开放的影响,探讨天麻成分对羟基苯甲醛的神经保护作用是否通过抑制钙通道的过度开放减轻钙超载,结果表明天麻成分对羟基苯甲醛可提高大鼠原代皮层神经元OGD/Rep损伤的存活率、减少NO的释放、降低胞内钙离子浓度、降低L型钙通道蛋白的表达。The rat primary cortical neurons oxygen-glucose deprivation/reintroduction( OGD/Rep) injury model was duplicated and was used to study the inhibitory effect of 4-hydroxybenzaldehyde on calcium channel. The cell viability was texted by MTT assay. The NO release was texted by nitric acid reductase assay. Intracellular calcium concentration was texted by flow cytometry and the protein and mRNA expressions of L-type calcium channel,NMDA receptor-type calcium channel and TRPM7 channel were texted by Western Blot and RT-PCR. The results indicated 4-hydroxybenzaldehydecan elevate survival rate of the primary cortical neuron which were affected by OGD/Rep injury,decrease NO release,reduce intracellular calcium iron concentration of the primary cortical neurons,as well as lower L channel protein expression.

关 键 词：对羟基苯甲醛 OGD/Rep 原代皮层神经元 钙通道 

分 类 号：R965.1[医药卫生—药理学]