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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