Effect and mechanism of ginsenoside Rg3 on inhibition of LLC proliferation in non-small cell lung cancer cells by immune checkpoint PD-L1
10.7501/j.issn.0253-2670.2019.01.025
- VernacularTitle: 人参皂苷Rg3调节免疫检查点PD-L1抑制肺癌Lewis细胞增殖的作用及机制研究
- Author:
Wei WANG
1
Author Information
1. Jiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, School of Pharmacy, Nanjing University of Chinese Medicine
- Publication Type:Journal Article
- Keywords:
Cell proliferation;
Ginsenoside Rg3;
Non-small cell lung cancer;
PD-L1;
PI3K/Akt/mTOR signal pathway
- From:
Chinese Traditional and Herbal Drugs
2019;50(1):166-171
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of ginsenoside Rg3 on immune checkpoint PD-L1 in Lewis cells (LLC) and to explore the related mechanism. Methods The effects of ginsenoside Rg3 on the proliferation of LLC were observed by MTT assay and cell long-term dynamic monitoring. LLC cells treated with 20 ng/mL IFN-γ were used to construct experimental model with high expression of PD-L1 in vitro. The effect of ginsenoside Rg3 on expression of PD-L1 was detected by flow cytometry and immunofluorescence. The effect of ginsenoside Rg3 on the protein expression of PI3K/Akt/mTOR pathway was verified by Western blotting. Results Ginsenoside Rg3 at 16, 32, 64, and 128 μmol/L significantly inhibited the proliferation of LLC (P < 0.01) and reduced the expression of PD-L1 induced by IFN-γ (P < 0.05). Ginsenoside Rg3 at 32 and 64 μmol/L significantly decreased the protein expression of PI3K and mTOR (P < 0.01), and ginsenoside Rg3 at 16, 32, and 64 μmol/L significantly inhibited the phosphorylation of Akt proteins (P < 0.05). Conclusion Ginsenoside Rg3 significantly inhibited the expression of PD-L1 in LLC cells by inhibiting PI3K/Akt/mTOR pathway. Ginsenoside Rg3 blocked the tumor cells escaping immune response by PD-L1 over-expression, enhanced the immune response of T cells, and inhibited the growth of non-small cell lung cancer cells.
