ArticleAnnals of translational medicine2020
Peroxiredoxin 6 overexpression regulates adriamycin-induced myocardial injury, oxidative stress and immune response in rats.
Article in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Peroxiredoxin 6 in Stress Orchestration and Disease Interplay.Antioxidants (Basel, Switzerland) · 2025Review
- Broadening horizons: The role of ferroptosis in myocardial ischemia-reperfusion injury.Naunyn-Schmiedeberg's archives of pharmacology · 2023Review
- Quercetin Alleviates the Immunotoxic Impact Mediated by Oxidative Stress and Inflammation Induced by Doxorubicin Exposure in Rats.Antioxidants (Basel, Switzerland) · 2021Article
- Transcription factor EB mediates oxidative stress-induced intervertebral disc degeneration via the NF-κB signaling pathway.Annals of translational medicine · 2021Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAdriamycin 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.
methodsSixty 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.
resultsThe 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.
conclusionsPRDX6 overexpression can alleviate adriamycin-induced myocardial injury in rats, which may be related to oxidative stress regulation and the levels of inflammatory factors.
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