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Skin-derived precursor Schwann cells protect SH-SY5Y cells against 6-OHDA-induced neurotoxicity by PI3K/AKT/Bcl-2 pathway.
Brain Research Bulletin ( IF 3.5 ) Pub Date : 2020-04-30 , DOI: 10.1016/j.brainresbull.2020.03.020
Ying Chen 1 , Jiabing Shen 1 , Chengxiao Ma 1 , Maosheng Cao 1 , Jianan Yan 1 , Jingjing Liang 1 , Kaifu Ke 2 , Maohong Cao 2 , Gu Xiaosu 2
Affiliation  

Skin-derived precursors (SKPs) are self-renewing and pluripotent adult stem cell sources that have been successfully obtained and cultured from adult tissues of rodents and humans. Skin-derived precursor Schwann cells (SKP-SCs), derived from SKPs when cultured in a neuro stromal medium supplemented with some appropriate neurotrophic factors, have been reported to play a neuroprotective effect in the peripheral nervous system. This proves our previous studies that SKP-SCs' function to bridge sciatic nerve gap in rats. However, the function of SKP-SCs in Parkinson disease (PD) remains unknown. This study was aimed to investigate the possible neuroprotective effects of SKP-SCs in 6-OHDA-induced Parkinson's disease (PD) model. Our results showed that the treatment with SKP-SCs prevented SH-SY5Y cells from 6-OHDA-induced apoptosis, accompanied by modulation of apoptosis-related proteins (Bcl-2 and Bax) and the decreased expression of active caspase-3. Furthermore, we confirmed that SKP-SCs might exert protective effects and increase the mitochondrial membrane potential (MMP) through PI3K/AKT/Bcl-2 pathway. Taken together, our results demonstrated that SKP-SCs protect against 6-OHDA-induced cytotoxicity through PI3K/AKT/Bcl-2 pathway in PD model in vitro, which provides a new theoretical basis for the treatment of PD.

中文翻译:

皮肤来源的前体雪旺氏细胞通过 PI3K/AKT/Bcl-2 通路保护 SH-SY5Y 细胞免受 6-OHDA 诱导的神经毒性。

皮肤源性前体 (SKP) 是自我更新和多能的成体干细胞来源,已从啮齿动物和人类的成体组织中成功获得和培养。据报道,皮肤源性前体雪旺氏细胞 (SKP-SCs) 在补充有一些合适的神经营养因子的神经基质培养基中培养时衍生自 SKP,据报道在周围神经系统中发挥神经保护作用。这证明了我们之前的研究表明 SKP-SCs 具有弥合大鼠坐骨神经间隙的功能。然而,SKP-SCs 在帕金森病 (PD) 中的功能仍然未知。本研究旨在研究 SKP-SCs 在 6-OHDA 诱导的帕金森病 (PD) 模型中可能的神经保护作用。我们的结果表明,SKP-SCs 处理阻止了 SH-SY5Y 细胞免受 6-OHDA 诱导的细胞凋亡,伴随着凋亡相关蛋白(Bcl-2 和 Bax)的调节和活性 caspase-3 的表达降低。此外,我们证实 SKP-SCs 可能通过 PI3K/AKT/Bcl-2 途径发挥保护作用并增加线粒体膜电位 (MMP)。总之,我们的结果表明,SKP-SCs 在体外 PD 模型中通过 PI3K/AKT/Bcl-2 通路保护 6-OHDA 诱导的细胞毒性,这为 PD 的治疗提供了新的理论基础。
更新日期:2020-04-30
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