Peripheral blood mesenchymal stem cells repair oxidative damage and apoptosis in an H2O2-induced vitiligo oxidative stress in vitro model via the IL-10-mediated PI3K/AKT pathway.

IF 3.4 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL
Rui-Lin Yang, Yi-Bing Yang, Han-Xiao Wei, Meng Zhang, Kang Yang, Yu-Jie Zhao, Wen Yan, Ying Yang, Tao Zhang
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引用次数: 0

Abstract

Peripheral blood mesenchymal stem cells (PBMSCs) are a less invasive and more accessible source of adult multipotent stem cells than bone marrow mesenchymal stem cells (BMMSCs), because their collection does not involve anaesthesia and the risk of complications. In the present study, we observed that PBMSCs alone exhibited a higher concentration of IL-10 in the supernatant when cultured independently. Furthermore, the supernatant from the Transwell co-culture system of PBMSCs with H2O2-induced oxidative stress in B16 melanoma cells, which serves as an in vitro model for vitiligo, demonstrated elevated levels of IL-10. Western blot analysis revealed that the PI3K/AKT signaling pathway was activated in B16 melanoma cells, as evidenced by increased phosphorylation of AKT, enhanced expression of the antioxidant enzyme HO-1 and the anti-apoptotic protein Bcl-2, alongside decreased expression of the pro-apoptotic proteins Bax and Cleaved-Caspase 3. Notably, these effects were inhibited by the IL-10 neutralizing antibody (AB9969) and the PI3K inhibitor (LY294002). Collectively, our findings suggest that PBMSCs may mitigate oxidative damage and apoptosis in B16 melanoma cells through the paracrine activation of the PI3K/AKT signaling pathway by IL-10. This approach offers a novel, readily available, and minimally invasive cellular therapeutic strategy for vitiligo while also providing a theoretical basis for targeting antioxidant pathways in treatment.

外周血间充质干细胞通过il -10介导的PI3K/AKT通路修复h2o2诱导的白癜风氧化应激模型中的氧化损伤和凋亡。
外周血间充质干细胞(PBMSCs)是一种比骨髓间充质干细胞(BMMSCs)侵入性更小、更容易获得的成体多能干细胞来源,因为它们的收集不涉及麻醉和并发症的风险。在本研究中,我们观察到PBMSCs单独培养时,上清液中IL-10的浓度更高。此外,作为白癜风的体外模型,PBMSCs与h2o2诱导的B16黑色素瘤细胞共培养系统的上清液显示IL-10水平升高。Western blot分析显示,在B16黑色素瘤细胞中,PI3K/AKT信号通路被激活,AKT磷酸化升高,抗氧化酶HO-1和抗凋亡蛋白Bcl-2表达增强,促凋亡蛋白Bax和Cleaved-Caspase 3表达降低。值得注意的是,这些作用被IL-10中和抗体(AB9969)和PI3K抑制剂(LY294002)所抑制。总之,我们的研究结果表明,PBMSCs可能通过IL-10对PI3K/AKT信号通路的旁分泌激活来减轻B16黑色素瘤细胞的氧化损伤和凋亡。该方法为白癜风提供了一种新颖、容易获得、微创的细胞治疗策略,同时也为靶向抗氧化途径的治疗提供了理论基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
European Journal of Medical Research
European Journal of Medical Research 医学-医学:研究与实验
CiteScore
3.20
自引率
0.00%
发文量
247
审稿时长
>12 weeks
期刊介绍: European Journal of Medical Research publishes translational and clinical research of international interest across all medical disciplines, enabling clinicians and other researchers to learn about developments and innovations within these disciplines and across the boundaries between disciplines. The journal publishes high quality research and reviews and aims to ensure that the results of all well-conducted research are published, regardless of their outcome.
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