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

Figure 4

Jaceosidin (4 mg/kg) reduced oxidative stress in doxorubicin- (DOX-) treated mice. (a–c) The mRNA levels of superoxide dismutase 1 (SOD1), SOD2, and glutathione peroxidase 1 (Gpx1) in the hearts (). (b) Total SOD activity in the hearts (). (e, f) Malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) levels in the hearts (). (g) The ratio of glutathione (GSH) to oxidized glutathione (GSSG) in jaceosidin-treated mice (). (h) Protein carbonyl content in jaceosidin-treated mice (). (i) The protein expression of nuclear factor E2-related factor 2 (Nrf2) and haem oxygenase-1 (HO-1) in jaceosidin-treated mice (). (j) Nrf2 activity (). 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, heart tissues were collected to assess myocardial oxidative damage, as reflected by (a–j). Data are shown as . Comparisons between multiple groups were performed using one-way ANOVA followed by a post hoc Bonferroni comparison analysis. compared with saline. compared with DOX alone.

(a)

(b)

(c)

(d)

(e)

(f)

(g)

(h)

(i)

(j)