Fig 2: Jaceosidin (4 mg/kg) did not provide cardiac protection in mice with sirtuin 1 (Sirt1) inhibition. (a) Ejection fraction (EF) in DOX-treated mice (n = 8 - 10). (b) The level of cardiac troponin I (cTnI) in DOX-treated mice (n = 6). (C) +dP/dt in DOX-treated mice (n = 6). (d) The levels of 4-hydroxynonenal (4-HNE) in DOX-treated mice (n = 6). (e, f) The levels of tumour necrosis factor- (TNF-) a and interleukin- (IL-) 6 in DOX-treated mice (n = 6). (g) The activity of caspase-3 in mice (n = 6). To inhibit Sirt1 in vivo, mice were subjected to a specific inhibitor of Sirt1 (Ex527, 1 mg/kg) every other day for a total of 8 days beginning 3 days before DOX injection. Data are shown as means ± SEM. Comparisons were performed using one-way ANOVA followed by a post hoc Bonferroni comparison analysis. *P < 0.05 versus the matched control.

Fig 3: Jaceosidin (4 mg/kg) inhibited doxorubicin- (DOX-) related cardiac injury in vivo. (a) Body weight (n = 12). (b) The ratio of heart weight (HW) to tibia length (TL) (n = 12). (c, d) The plasma levels of cardiac troponin I (cTnI) and lactate dehydrogenase (LDH) (n = 12). (e) Ejection fraction (EF) in the mice (n = 8). (f, g) Left ventricular end-diastolic pressure (LVEDP) and the alteration in +dP/dt (n = 8). (h) The alteration in stroke work (n = 8). (i) Cardiomyocytes vacuolization were evaluated by HE staining. Mice were intraperitoneally injected with a single dose of DOX (15 mg/kg) to establish the acute cardiac injury model. Five days after DOX injection, blood samples and heart tissues were collected to assess cardiac injury, as reflected by (a–h). Data are shown as means ± SEM. Comparisons between multiple groups were performed using one-way ANOVA followed by a post hoc Bonferroni comparison analysis. *P < 0.05 compared with saline. #P < 0.05 compared with DOX alone.