Effects of Gentiopicroside on Oxidative Stress and Apoptosis in Gastric Cancer Cells

Gastric cancer (GC) cells were sorted into six groups: NC, different concentrations of gentiopicroside, pcDNA-NC, pcDNA-Nrf2, pcDNA-NC+ gentiopicroside, and pcDNA-Nrf2+ gentiopicroside. The detection and comparison of cell survival and apoptosis showed that the activity of GC cells decreased and the apoptosis rate increased after gentiopicroside treatment. Western blot detection was performed to determine the expression levels of proliferating cell nuclear antigen (PCNA), B-cell leukemia/lymphoma-2 (Bcl-2)-associated X protein (Bax), Bcl-2, Kelch-like epichlorohydrinassociated protein 1 (Keap1), nuclear factor erythroid 2-related factor 2 (Nrf2), and antioxidant response element (ARE). Kits were used to determine the malondialdehyde (MDA) content, super-oxide dismutase (SOD) activity, and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity. The MDA content, NADPH oxidase activity, and Keap1 and Bax expression levels increased, and the SOD activity and Bcl-2, PCNA, Nrf2, and ARE expression levels decreased. Nrf2 overexpression increased the cell activity, SOD activity, and Nrf2, ARE, PCNA, and Bcl-2 expression levels and reduced the apoptosis rate, MDA content, NADPH oxidase activity, and Bax and Keap1 expression levels. At the same time, Nrf2 overexpression reversed the effects of gentiopicroside on oxidative stress and apoptosis of GC cells. These results suggest that gentiopicroside probably promotes oxidative stress and apoptosis of GC cells by inhibiting the Keap1/Nrf2/ARE signaling pathway.