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中华变种对HO诱导的皮质神经元氧化应激和线粒体功能障碍的神经治疗作用。

Neurotherapeutic Effect of var. Chinensis against HO-Induced Oxidative Stress and Mitochondrial Dysfunction in Cortical Neurons.

作者信息

Hong Jin Young, Kim Hyunseong, Lee Junseon, Jeon Wan-Jin, Baek Seung Ho, Ha In-Hyuk

机构信息

Jaseng Spine and Joint Research Institute, Jaseng Medical Foundation, Seoul 135-896, Korea.

College of Korean Medicine, Dongguk University, 32 Dongguk-ro, Ilsandong-gu, Goyang-si 10326, Korea.

出版信息

Antioxidants (Basel). 2021 Mar 3;10(3):375. doi: 10.3390/antiox10030375.

DOI:10.3390/antiox10030375
PMID:33802485
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8001496/
Abstract

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 (HO)-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 HO-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.

摘要

中华变种(IBC)一直被用作治疗炎症性疾病的传统草药。尽管其抗炎和抗氧化作用已有报道,但IBC在皮质神经元中是否发挥神经保护作用及其相关机制仍不清楚。在本研究中,我们使用过氧化氢(HO)诱导的损伤模型,研究了不同浓度的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,IBC可以通过抑制线粒体ROS生成并提高HO处理神经元中的三磷酸腺苷水平,在体外模拟的活性氧(ROS)生成条件下有效增强神经元活力。此外,我们证实,通过改善线粒体膜电位状态和调节与细胞死亡相关的蛋白质细胞色素c的表达,可减轻神经元死亡。此外,IBC增加了脑源性神经营养因子和神经生长因子的表达。此外,IBC抑制了主要突触囊泡蛋白突触素的丢失并诱导其产生。本研究首次证明,IBC通过减少线粒体相关的氧化应激和改善线粒体功能障碍发挥其神经保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/f74d8323c5d4/antioxidants-10-00375-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/2be9e8583a0c/antioxidants-10-00375-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/78212139eaca/antioxidants-10-00375-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/8a448610801a/antioxidants-10-00375-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/ec2cb87d7860/antioxidants-10-00375-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/62f90de3c971/antioxidants-10-00375-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/b051c5b147e9/antioxidants-10-00375-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/0332a4ebdec1/antioxidants-10-00375-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/6aca176b893a/antioxidants-10-00375-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/918b4f28715b/antioxidants-10-00375-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/f74d8323c5d4/antioxidants-10-00375-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/2be9e8583a0c/antioxidants-10-00375-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/78212139eaca/antioxidants-10-00375-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/8a448610801a/antioxidants-10-00375-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/ec2cb87d7860/antioxidants-10-00375-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/62f90de3c971/antioxidants-10-00375-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/b051c5b147e9/antioxidants-10-00375-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/0332a4ebdec1/antioxidants-10-00375-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/6aca176b893a/antioxidants-10-00375-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/918b4f28715b/antioxidants-10-00375-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e29/8001496/f74d8323c5d4/antioxidants-10-00375-g010.jpg

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