Reducing oxidative stress may be important for treating pirarubicin‑induced cardiotoxicity with schisandrin B

Figure 1. SchB improves THP-induced body weight, food intake and echocardiographic changes in rats. (A) Body weights and (B) food intake of THP-treated rats decreased in the third and fourth weeks. (C) EF and (D) %FS decreased, and (E) LVIDd and (F) LVIDs increased in THP-treated rats. After treatment with SchB, the aforementioned changes were effectively alleviated. All values are presented as the mean ± SD. *P<0.05 vs. CON; #P<0.05 vs. THP. EF, left ventricular ejection fraction; FS, left ventricular shortening fraction; LVIDd, left ventricular internal diameter at end-diastole; LVIDs, left ventricular internal diameter at end-systole; CON, control; SchB, schisandrin B; THP, pirarubicin.

Figure 2. SchB effectively improves THP-induced myocardial injury in rats. The (A) R wave and (B) S wave increased; the (C) T wave decreased; and the (D) QT interval was prolonged in THP-treated rats. Similarly, (E) LDH, (F) BNP, (G) CK-MB and (H) cTnT increased in the serum of THP-treated rats. After SchB treatment, the aforementioned changes were significantly improved. All values are presented as the mean ± SD. *P<0.05 vs. CON; #P<0.05 vs. THP. LDH, lactate dehydrogenase; BNP, brain natriuretic peptide; CK-MB, creatine kinase MB; cTnT, and cardiac troponin T; CON, control; SchB, schisandrin B; THP, pirarubicin.

Figure 3. SchB attenuates THP-induced oxidative stress in rats. (A and E) MDA content increased and the (B and F) SOD content decreased in both serum and heart tissue. SchB also increased the THP-induced decrease in (C and G) CAT and (D and H) T-AOC. All values are presented as the mean ± SD. *P<0.05 vs. CON; #P<0.05 vs. THP. SOD, superoxide dismutase; MDA, malondialdehyde; CAT, catalase; T-AOC, total antioxidant capacity; CON, control; SchB, schisandrin B; THP, pirarubicin.

Figure 4. SchB improves myocardial tissue changes induced by THP in rats. (A) The myocardial cells in the THP group were disordered, the intercellular space was increased and the myocardial tissue was calcified or denatured. However, these changes in the heart were alleviated after SchB treatment (magnification, x200). (B) The expression levels of SOD2, pro-caspase-3 and Bcl-2/Bax decreased, while the expression levels of NOX2 and cleaved-caspase-3 increased. However, after treatment with SchB, the aforementioned changes were significantly improved. (C) Semi-quantitative analysis of western blotting results. Magnification, x200. All values are presented as the mean ± SD. *P<0.05 vs. CON; #P<0.05 vs. THP. SOD, superoxide dismutase; NOX, NADPH oxidase; CON, control; SchB, schisandrin B; THP, pirarubicin.

Figure 5. SchB attenuates THP-induced oxidative stress in primary cardiomyocytes. THP reduced H9C2 (A) cardiomyocyte viability and (B) increased reactive oxygen species. Scale bar, 200 µm. (C) Similarly, the expression levels of SOD2, pro-caspase-3 and Bcl-2/Bax decreased, while the expression levels of NOX2 and cleaved-caspase-3 increased. However, after treatment with SchB, the aforementioned changes were significantly improved. (D) Semi-quantitative analysis of western blotting results. All values are presented as the mean ± SD. *P<0.05 vs. CON; #P<0.05 vs. THP. SOD, superoxide dismutase; NOX, NADPH oxidase; CON, control; SchB, schisandrin B; THP, pirarubicin.