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首页> 外文期刊>Acta neurobiologiae experimentalis >The differential effects of neuroleptic drugs and PACAP on the expression of BDNF mRNA and protein in a human glioblastoma cell line
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The differential effects of neuroleptic drugs and PACAP on the expression of BDNF mRNA and protein in a human glioblastoma cell line

机译：神经糖尿病药物和PACAP对人胶质细胞瘤细胞系BDNF mRNA和蛋白表达的差异影响

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It has been suggested that, in addition to modulation of monoaminergic neurotransmission, antipsychotic drugs can also affect expression of neurotrophic factors in the brain. The present study was aimed to examine the effects of the first generation neuroleptic drug (FGA; haloperidol) and second generation neuroleptic drugs (SGAs; olanzapine and amisulpride) on expression and level of brain-derived neurotrophic factor (BDNF) in astrocyte-like T98G glioblastoma cell line. Effects of these drugs were compared to the action of PACAP38, a neuropeptide with well known BDNF-mediated neuroprotective effects. The tested neuroleptics differentially regulated the mRNA expression and protein level of BDNF depending on the concentration and incubation time. Using rtPCR technique, we demonstrate that, from the three tested neuroleptics, both haloperidol as well as olanzapine at 5 mu M concentration (but not at 20 mu M) increased BDNF mRNA expression with a similar efficacy after a 72 h incubation. In order to confirm the observed changes in the mRNA expression of BDNF, a protein expression assay was performed. The exposure of cells only to 5 mu M olanzapine for 72 h increased BDNF concentration in the culture medium by 29%. Additionally, PACAP significantly up-regulated BDNF mRNA expression in T98G cells and the obtained results correlated positively with the increased production of BDNF protein, by 22% above control. The results of the paper show that olanzapine, similarly to exogenous PACAP38, increased BDNF mRNA expression and protein release, which can contribute to its neuroprotective mechanism of action in the cells of nonneuronal origin. The results of the present paper confirm the findings that BDNF may represent the key target for olanzapine and PACAP.
机译：已经提示，除了调制单氨基能神经递质之外，抗精神病药还可以影响大脑中神经营养因子的表达。目前的研究旨在检测第一代神经抑制药物（FGA;氟哌啶醇）和第二代神经抑制药物（SGAS;奥氮藻和氨基丙烯酯）对星形胶质细胞样T98G的表达和水平的影响胶质母细胞瘤细胞系。将这些药物的效果与PACAP38，神经肽的作用进行比较，具有众所周知的BDNF介导的神经保护作用。测试的神经抑制剂根据浓度和孵育时间差异调节BDNF的mRNA表达和蛋白质水平。使用RTPCR技术，我们证明，从三个测试的神经抑制剂，氟哌啶醇以及5μm浓度（但不在20μm）的奥拉齐滨增加，在72小时孵育后，在具有相似的功效增加BDNF mRNA表达。为了确认BDNF的mRNA表达的观察到的变化，进行蛋白质表达测定。仅将细胞暴露于5μm奥沙坦滨72小时，将培养基中的BDNF浓度增加29％。另外，PACAP在T98G细胞中显着上调BDNF mRNA表达，得到的结果随着BDNF蛋白的产量增加而相关的，对照的增加22％。本文的结果表明，奥氮翼同样地与外源性PACAP38增加，增加了BDNF mRNA表达和蛋白质释放，这可以有助于非生物元素细胞中的神经保护机制。本文的结果证实了BDNF可以代表奥兰扎滨和PACAP的关键靶标的结果。

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