Research Article

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

Figure 2

Jaceosidin inhibited the inflammatory response and cell loss in vitro. (a) Nuclear factor kappa-B (NF-κB) binding activity (). (b, c) The mRNA levels of inflammatory factors (). (d) Cell viability after doxorubicin (DOX) treatment (). (e, f) The release of lactate dehydrogenase (LDH) and creatine kinase (CK) in cells (). For (a–f), 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 inflammatory markers (a–f) 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.
(a)
(b)
(c)
(d)
(e)
(f)