Abstract
Cardiotoxicity has been corroborated to be the toxic influence of cisplatin (CDDP). Oxidative stress and cardiomyocyte apoptosis play a vital part in cardiotoxicity induced by CDDP. Salvianolic acid Salvianolic acid B (SalB) is a monomeric component of Salvia miltiorrhiza, which has antioxidant and anti-inflammatory influences. In this research, we explored the mechanism of SalB in cardiotoxicity induced by CDDP. 36 Wistar rats were separated into sham subgroup, CDDP (10 mg/kg) subgroup, CDDP (10 mg/kg) + SalB (1 μM) subgroup at random, CDDP (10 mg/kg) + SalB (5 μM) subgroup and CDDP (10 mg/kg) + SalB (10 μM) subgroup, Nicotinic Acid Riboside (NAR, 5 μM), with 6 rats in each subgroup. The cardiac function of rats in each subgroup was estimated by echocardiography, and hematoxylin-eosin (HE) staining and Masson staining corroborated the pathological changes of cardiac tissue. Biochemical kits were utilized for detecting the lactate dehydrogenase (LDH), creatine kinase (CK), interleukin-1β (IL-1β), IL-18, and caspase-1 concentrations in serum, superoxide dismutase (SOD), and malondialdehyde (MDA) in myocardial tissue, TdT-mediated dUTP Nick-End Labeling (TUNEL) staining, and flow cytometry were utilized for estimating the apoptosis level in myocardial tissue, western blot was used for estimating caspase-3, Bcl2-Associated X (Bax) levels in myocardial tissue and proteins levels related to Nuclear factor E2 related factor 2 (Nrf2) signal pathway. CDDP-induced cardiac dysfunction, myocardial injury, boosted LDH and CK levels in serum (p < 0.05), memorably increased oxidative stress level in myocardial tissue (p < 0.05), boosted inflammatory response (p < 0.05), boosted apoptosis rate of cardiomyocytes (p < 0.05), and declined the Nrf2, NAD(P)H quinone oxidoreductase 1 (NQO1), heme oxygenase 1 (HO-1) protein levels (p < 0.05). Interestingly, SalB remedy could alleviate the changes caused by CDDP in the above parameters, significantly decrease the level of myocardial oxidative stress and apoptosis (p < 0.05). SalB ameliorates the injury of cardiomyocytes induced by chemotherapy through oxidative stress mediated by the Nrf2/antioxidant response element (ARE) signal pathway.
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