Background:Adriamycin is an anthracycline drug used to treat a variety of tumors. Adriamycin has a much stronger affinity for myocardial tissue than other body tissues. Cancer patients treated with adriamycin are prone to toxic damage to heart tissue. Peroxiredoxin 6 (PRDX6) is a novel antioxidant enzyme in metabolic diseases, the aim of this study was to investigate the role of PRDX6 in myocardial injury.
Methods:Sixty male specific-pathogen-free Wistar rats were enrolled and divided equally into the control group (control), the Adriamycin group, the Adriamycin + empty vector lentivirus (Adriamycin + LV) group, and the Adriamycin + Peroxiredoxin 6 overexpression (Adriamycin + PRDX6) group. Western blot, reverse transcription-polymerase chain reaction (PCR), enzyme-linked immunosorbent assay, hematoxylin and eosin staining (HE) and immunohistochemistry were used in this research.
Results:The myocardial tissues of the Adriamycin group had significantly lower expression levels of PRDX6 and PRDX6 mRNA than those of the control group, and the myocardial tissues of the Adriamycin + PRDX6 rats had significantly higher expression levels of PRDX6 and PRDX6 mRNA than those of the Adriamycin + LV group. Serum creatine kinase isoenzyme (CK-MB), myoglobin (Mb), cardiac troponin I (cTnI), myocardial injury, positive rate of caspase-3, B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (Bax) levels, malondialdehyde (MDA), lactate dehydrogenase (LDH), IL-1β, IL-6, inducible nitric oxide synthase (iNOS), and IL-4 proteins in the adriamycin-induced rats were significantly higher than those in the control group, while superoxide dismutase (SOD) activity was significantly lower than that in the control group. PRDX6 overexpression reversed the above results.
Conclusions:PRDX6 overexpression can alleviate adriamycin-induced myocardial injury in rats, which may be related to oxidative stress regulation and the levels of inflammatory factors.
