Shokrzadeh M, Ataee R, habibi E, Rahmati Kukandeh M, Alizade Chapi M, Asemi S et al . Protective effects of hydroalcoholic extract of ginger on DNA damage and viability of PC12 cells exposed to sodium dithionite. J Mazandaran Univ Med Sci 2025; 35 (249) :32-44
URL:
http://jmums.mazums.ac.ir/article-1-21197-en.html
Abstract: (24 Views)
Background and purpose: This study focused on sodium dithionite, a chemical widely used in various industries, which causes oxidative damage to cells and DNA. Considering the well-known antioxidant properties of ginger, the research investigated the effects of hydroalcoholic ginger extract on genetic damage and cell viability. The study specifically evaluated how the extract influenced genetic disorders and improved the survival of PC12 cells that were exposed to the harmful effects of sodium dithionite.
Materials and methods: In this experimental study, PC12 cells were treated with varying concentrations of ginger extract (200, 400, and 600 mg/ml) together with sodium dithionite at its IC50 concentration. Following exposure, cell viability was evaluated using the MTT assay to determine the extract’s protective effects. Additionally, DNA damage was quantified using the alkaline Comet assay, which provided insights into the genotoxic effects of sodium dithionite and the potential reduction by ginger extract. All data were statistically analyzed using GraphPad Prism software, with a significance threshold set at p < 0.05 to identify meaningful differences between treated and control groups.
Results: The results showed that ginger extract in the maximum concentration (600 mg/ml) maintains cell survival (P<0.001). In addition, the extract caused a significant reduction in DNA damage, and this effect was the most pronounced at the high concentration (600 mg/ml) (P<0.001).
Conclusion: The hydroalcoholic extract of ginger exhibits protective effects against oxidative damage induced by sodium dithionite in PC12 cells. These results indicate that ginger can be used as a protective agent against damage caused by oxidative stress.