Ginsenoside Rg3 regulates sensitization effect of superoxide dismutase on thyroid cancer photodynamic therapy via antioxidant response element signaling pathway

IF 0.7 4区 材料科学 Q3 Materials Science Materials Express Pub Date : 2023-09-01 DOI:10.1166/mex.2023.2491
Yanhui Yin, Qing Li, Yunlong Zhang
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Abstract

Clinical studies have shown that, ginsenoside Rg3 has strong antitumor and antioxidant effects. Therefore, this study used ginsenoside Rg3 to explore its role in the antioxidant response element (ARE) signaling pathway, to clarify the mechanism of regulating superoxide dismutase (SOD) and enhancing sensitivity of cancer cells to photodynamic therapy, providing a basis for improving clinical treatment effect. A papillary thyroid carcinoma mouse model was constructed and divided into study groups, followed by Ki-67 and TUNEL (Terminal deoxynucleotidyl transferase dUTP nick end labeling) staining, CCK-8 method and flow cytometry analysis. Level of reactive oxygen species, and ARE and SOD were assessed by qRT-PCR (quantificational rt-PCR) and Western blot. No mouse death occurred during model establishment and intervention, and the tumor formation rate was 100%. Moreover, the Ki-67 positive cells in tumor tissues from the ginsenoside Rg3 group were lowest, indicating tumor growth was inhibited; while the TUNEL cells were increased, indicating that tumor cells underwent apoptosis. Meanwhile, BCPAP (Human Thyroid Cancer Papillary Cell) proliferation and migration in the ginsenoside Rg3 group were lower than in the ARE inhibitor group, while apoptotic ability was increased. The levels of ARE and SOD in the ginsenoside Rg3 group were also increased. Ginsenoside Rg3 plays an anti-tumor effect through ARE signaling pathway and accelerates cell apoptosis. At the same time, the Ginsenoside Rg3 can enhance ROS activity, upregulate ARE and SOD, and increase the sensitivity of cancer cells to photodynamic therapy.
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人参皂苷Rg3通过抗氧化反应元件信号通路调控超氧化物歧化酶对甲状腺癌光动力治疗的增敏作用
临床研究表明,人参皂苷Rg3具有较强的抗肿瘤和抗氧化作用。因此,本研究利用人参皂苷Rg3探讨其在抗氧化反应元件(ARE)信号通路中的作用,阐明其调节超氧化物歧化酶(SOD)、增强癌细胞对光动力治疗敏感性的作用机制,为提高临床治疗效果提供依据。构建甲状腺乳头状癌小鼠模型,分为研究组,采用Ki-67和TUNEL(末端脱氧核苷酸转移酶dUTP缺口末端标记)染色、CCK-8法和流式细胞术分析。采用qRT-PCR(定量rt-PCR)和Western blot检测各组小鼠活性氧、ARE和SOD水平。在模型建立和干预过程中均无小鼠死亡,肿瘤形成率为100%。人参皂苷Rg3组肿瘤组织中Ki-67阳性细胞数最低,表明人参皂苷Rg3组肿瘤生长受到抑制;TUNEL细胞增多,提示肿瘤细胞发生凋亡。同时,人参皂苷Rg3组的BCPAP(人甲状腺癌乳头状细胞)增殖和迁移均低于ARE抑制剂组,细胞凋亡能力增强。人参皂苷Rg3组ARE、SOD水平升高。人参皂苷Rg3通过ARE信号通路发挥抗肿瘤作用,加速细胞凋亡。同时人参皂苷Rg3可以增强ROS活性,上调ARE和SOD,增加癌细胞对光动力治疗的敏感性。
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来源期刊
Materials Express
Materials Express NANOSCIENCE & NANOTECHNOLOGY-MATERIALS SCIENCE, MULTIDISCIPLINARY
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0.00%
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69
审稿时长
>12 weeks
期刊介绍: Information not localized
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