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Oxidative Stress Mediates Anti-proliferative Effects of Nifedipine on AGS Cells

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Previous studies have demonstrated the anticancer properties of certain calcium channel blockers when administered as sole agents. This exploration aimed to explore the potential anti-proliferative activity of nifedipine on AGS gastric cancer cells and to determine the contribution of oxidative stress in mediating this response. To assess the anti-proliferative impact of nifedipine, AGS cell viability was calculated employing the XTT assay across a concentration range of 25, 50, 100, 200, and 500 µg/mL. Concurrently, TAS and TOS kits were employed to evaluate the drug's influence on oxidative stress levels. Nifedipine exhibited a concentration-dependent cytotoxic effect on AGS cells, with a statistically significant reduction in cell viability. The IC50 value for AGS cells after 24 hours was determined to be 98.49 µg/mL. At this concentration, a substantial augmentation in TOS and a concurrent diminution in TAS levels were observed relative to the control group. These observations imply that nifedipine-induced oxidative stress is one of the mechanisms underlying its cytotoxic action against gastric cancer cells. Our results highlight the potential therapeutic utility of nifedipine in this cancer type.
Title: Oxidative Stress Mediates Anti-proliferative Effects of Nifedipine on AGS Cells
Description:
Previous studies have demonstrated the anticancer properties of certain calcium channel blockers when administered as sole agents.
This exploration aimed to explore the potential anti-proliferative activity of nifedipine on AGS gastric cancer cells and to determine the contribution of oxidative stress in mediating this response.
To assess the anti-proliferative impact of nifedipine, AGS cell viability was calculated employing the XTT assay across a concentration range of 25, 50, 100, 200, and 500 µg/mL.
Concurrently, TAS and TOS kits were employed to evaluate the drug's influence on oxidative stress levels.
Nifedipine exhibited a concentration-dependent cytotoxic effect on AGS cells, with a statistically significant reduction in cell viability.
The IC50 value for AGS cells after 24 hours was determined to be 98.
49 µg/mL.
At this concentration, a substantial augmentation in TOS and a concurrent diminution in TAS levels were observed relative to the control group.
These observations imply that nifedipine-induced oxidative stress is one of the mechanisms underlying its cytotoxic action against gastric cancer cells.
Our results highlight the potential therapeutic utility of nifedipine in this cancer type.

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