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首页> 外文期刊>RSC Advances >Neuroprotective effects of myristargenol A against glutamate-induced apoptotic HT22 cell death
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Neuroprotective effects of myristargenol A against glutamate-induced apoptotic HT22 cell death

机译：Myristargenol A对谷氨酸诱导的凋亡性HT22细胞死亡的神经保护作用

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Glutamate is an important neurotransmitter in the central nervous system; however, at high concentrations, it causes excitotoxicity and many neurological disorders. Excitotoxicity induces cell death by apoptosis. Thus, factors that can inhibit the apoptotic pathways are a target of drug development for the treatment and prevention of neurodegenerative diseases. Herein, the antioxidative and neuroprotective effects of myristargenol A were examined in glutamate-induced mouse hippocampal neuronal HT22 cells. When the HT22 cells were stressed with glutamate, cell viability decreased to 44.4 ± 5.6% when compared with the case of the control cells (100 ± 4.8%); however, when these cells were treated with myristargenol A (10 μM), the cell viability was increased by 113.6 ± 2.3%. The protective effect of myristargenol A against the apoptosis of glutamate-induced HT22 cells was also confirmed using FITC-annexin V/propidium iodide double staining. In addition, myristargenol A protected the mitochondrial membrane potential (Δ Ψ _(m) ). Subsequently, the expression levels of proteins in the caspase pathway related with the induction of apoptosis were decreased. Moreover, the expression levels of mitochondrial-related proteins, such as Bcl-2 and Bax, were examined, and it was found that the expression ratio of Bax/Bcl-2 decreased. In addition, myristargenol A inhibited the activity of mitogen-activated protein kinases, including p38 and c-Jun N-terminal kinase, for an oxidative stress protection effect but increased the activity of the extracellular signal-regulated kinases 1 and 2 for cell proliferation. These results reveal that myristargenol A possesses a neuroprotective effect against the neuronal cell damage caused by glutamate.
机译：谷氨酸是中枢神经系统中重要的神经递质。但是，高浓度时会引起兴奋性毒性和许多神经系统疾病。兴奋毒性通过凋亡诱导细胞死亡。因此，可以抑制凋亡途径的因子是用于治疗和预防神经变性疾病的药物开发的目标。在本文中，在谷氨酸诱导的小鼠海马神经元HT22细胞中检查了美斯达新酚A的抗氧化和神经保护作用。当谷氨酸对HT22细胞施加压力时，与对照细胞（100±4.8％）相比，细胞活力下降至44.4±5.6％;但是，当用Mystarstargenol A（10μM）处理这些细胞时，细胞活力提高了113.6±2.3％。使用FITC-annexin V /碘化丙啶双重染色也证实了Mystarargenol A对谷氨酸诱导的HT22细胞凋亡的保护作用。此外，Mystarargenol A保护线粒体膜电位（Δ_（m））。随后，与凋亡诱导有关的胱天蛋白酶途径中蛋白质的表达水平降低。此外，检查了线粒体相关蛋白例如Bcl-2和Bax的表达水平，发现Bax / Bcl-2的表达比例降低。此外，Mystarargenol A抑制包括p38和c-Jun N端激酶在内的丝裂原活化蛋白激酶的活性，具有氧化应激保护作用，但增加了细胞外信号调节激酶1和2的细胞增殖活性。这些结果表明，Mystarargenol A对谷氨酸引起的神经细胞损伤具有神经保护作用。

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