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首页> 外文期刊>CNS neuroscience & therapeutics. >Olanzapine induced autophagy through suppression of NF‐κB activation in human glioma cells
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Olanzapine induced autophagy through suppression of NF‐κB activation in human glioma cells

机译：奥氮平通过抑制人脑胶质瘤细胞中NF-κB的活化而诱导自噬

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Aims Our laboratory previously reported that olanzapine treatment inhibited growth of glioma cell lines and hypothesized that autophagy may be involved in the proliferation inhibitory effects of olanzapine. However, the mechanisms of olanzapine‐contributed autophagy activation are unclear. Methods The inhibitory effects of olanzapine on glioma cells were evaluated by CCK8 assay, Hoechst 33258 staining and annexin V‐FITC/PI staining. Western blotting, nuclear separation techniques, and immunofluorescence assays were used to investigate the relationship between the inhibition of NF‐κB and autophagy activation by olanzapine. Results In this work, we verified that olanzapine increased autophagic flux and autophagic vesicles. In addition, we confirmed that autophagy was related to NF‐κB inhibition in cancer progression, especially with the nuclear translocation of p65. Furthermore, we demonstrated that autophagy induced by olanzapine could be impaired with TNFα cotreatment. We also found that olanzapine had an inhibitory effect on T98 cells with positive MGMT protein expression, which may involve the inhibition of MGMT through effects on NF‐κB. Conclusions Our findings identify a pathway by which olanzapine induces autophagy by depressing NF‐κB in a glioma cell line, providing evidence which supports the use of olanzapine as a potential anticancer drug.
机译：目的我们的实验室先前曾报道奥氮平治疗可抑制神经胶质瘤细胞系的生长，并假设自噬可能与奥氮平的增殖抑制作用有关。然而，奥氮平促进自噬激活的机制尚不清楚。方法采用CCK8法，Hoechst 33258染色和Annexin V-FITC / PI染色评价奥氮平对神经胶质瘤细胞的抑制作用。使用Western印迹，核分离技术和免疫荧光分析法研究了奥氮平对NF-κB抑制与自噬激活之间的关系。结果在这项工作中，我们证实了奥氮平增加了自噬通量和自噬囊泡。此外，我们证实自噬与癌症进展中NF-κB抑制有关，特别是与p65的核易位有关。此外，我们证明了奥氮平诱导的自噬可能受到TNFα协同治疗的损害。我们还发现奥氮平对MGMT蛋白表达阳性的T98细胞具有抑制作用，这可能涉及通过对NF-κB的作用来抑制MGMT。结论我们的发现确定了奥氮平通过抑制神经胶质瘤细胞系中的NF-κB诱导自噬的途径，提供了支持将奥氮平用作潜在抗癌药的证据。

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