Inula britannica var. chinensis (IBC) has been used as a traditional medicinal herb to treat inflammatory diseases. Although its anti-inflammatory and anti-oxidative effects have been reported, whether IBC exerts neuroprotective effects and the related mechanisms in cortical neurons remain unknown. In this study, we investigated the effects of different concentrations of IBC extract (5, 10, and 20 µg/mL) on cortical neurons using a hydrogen peroxide (H2O2)-induced injury model. Our results demonstrate that IBC can effectively enhance neuronal viability under in vitro-modeled reaction oxygen species (ROS)-generating conditions by inhibiting mitochondrial ROS production and increasing adenosine triphosphate level in H2O2-treated neurons. Additionally, we confirmed that neuronal death was attenuated by improving the mitochondrial membrane potential status and regulating the expression of cytochrome c, a protein related to cell death. Furthermore, IBC increased the expression of brain-derived neurotrophic factor and nerve growth factor. Furthermore, IBC inhibited the loss and induced the production of synaptophysin, a major synaptic vesicle protein. This study is the first to demonstrate that IBC exerts its neuroprotective effect by reducing mitochondria-associated oxidative stress and improving mitochondrial dysfunction.
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机译：Inula Britannica var。 Chinensis（IBC）已被用作传统药草以治疗炎症性疾病。虽然据报道了其抗炎和抗氧化作用，但IBC是否施加神经保护作用，并且皮质神经元中的相关机制仍然未知。在该研究中，我们研究了使用过氧化氢（H2O2）损伤模型的不同浓度IBC提取物（5,10和20μg/ mL）对皮质神经元的影响。我们的结果表明，通过抑制线粒体ROS产生和增加H2O2处理的神经元的腺苷三磷酸水平，IBC可以有效地提高了体外模拟的反应氧物质（ROS） - 生成条件下的神经元活力。另外，我们证实通过改善线粒体膜电位状态并调节细胞色素C的表达，与细胞死亡有关的蛋白质的表达，证实神经元死亡。此外，IBC增加了脑衍生的神经营养因子和神经生长因子的表达。此外，IBC抑制了损失并诱导了突触囊泡蛋白的突触蛋白的产生。本研究首先证明IBC通过降低线粒体相关的氧化应激和改善线粒体功能障碍来施加其神经保护作用。
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