Protection against Doxorubicin-Related Cardiotoxicity by Jaceosidin Involves the Sirt1 Signaling Pathway

Figure 1

Jaceosidin inhibited reactive oxygen species (ROS) production in doxorubicin- (DOX-) treated cells. (a–c) The production of ROS, hydrogen peroxide, and superoxide in jaceosidin-treated cells (). (d) Malondialdehyde (MDA) content in jaceosidin-treated cells (). (e) The ratio of glutathione (GSH) to oxidized glutathione (GSSG) in jaceosidin-treated cells (). (f) Total superoxide dismutase (SOD) activity in DOX-treated cells. (g) Protein carbonyl content in the indicated groups (). For (a–g), cells were pretreated with various concentrations of jaceosidin (0, 2.5, 5, 10, 15 μmol/l) 6 hours before DOX (1 μmol/L) administration. The oxidative stress markers (a–g) were detected 24 hours after DOX administration. Data are shown as . Comparisons between multiple groups were performed using one-way ANOVA followed by a post hoc Bonferroni comparison analysis. compared with control. compared with DOX alone.

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