ArticleOxidative medicine and cellular longevity2022
Effects of Peroxiredoxin 6 and Its Mutants on the Isoproterenol Induced Myocardial Injury in H9C2 Cells and Rats.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Peroxiredoxin-6 protects against oxidative stress-mediated hypertrophic remodeling in JPH2-A399S knock-in mice.International journal of cardiology. Heart & vasculature · 2026Article
- Linking Experimental Models to Pathophysiology: Oxidative Stress and DNA Damage in Cardiovascular Diseases.International journal of molecular sciences · 2026Review
- Multi-Target Cardioprotection fromAntioxidants (Basel, Switzerland) · 2026Article
- The effect of carvacrol on kidney injury caused by isopreterenol-induced myocardial infarction.BMC nephrology · 2025Article
- Peroxiredoxin 6 in Stress Orchestration and Disease Interplay.Antioxidants (Basel, Switzerland) · 2025Review
- α-Amanitin aggravates hepatic injury by activating oxidative stress and mitophagy via peroxiredoxin 6 inhibition.Immunologic research · 2025Article
- Synergistic effects of ginsenoside Rb1 and peroxiredoxin 6 in enhancing myocardial injury treatment through anti-inflammatory, anti-oxidative, and anti-apoptotic mechanisms.Journal of ginseng research · 2025Article
- Ciprofol attenuates the isoproterenol-induced oxidative damage, inflammatory response and cardiomyocyte apoptosis.Frontiers in pharmacology · 2022Article
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6 authors.
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Abstract
Background: Peroxiredoxin 6 (PRDX6) is an important antioxidant enzyme, with a potential application value in the treatment of diseases caused by oxidative damage. Methods: PRDX6 and a mutant (mPRDX6) were heterologously expressed by using an E.coli expression system and purified by Ni-affinity chromatography. Isoproterenol (ISO) was used to induce a myocardial cell injury model and an animal myocardial injury model. After the treatment with PRDX6 and mPRDX6, the proliferation activity of H9C2 cells was detected by Cell Counting Kit-8 (CCK8) method; the apoptosis was evaluated by flow cytometry, and the histological changes of myocardial cells were observed by hematoxylin and eosin (H&E) staining, the levels of catalase (CAT), glutathione peroxidase (GPX), malondialdehyde (MDA), and superoxide dismutase (SOD) in ISO-treated H9C2 cells as well as in the heart tissue and serum of rats treated with ISO were detected, and the expression levels of Bax, Bcl-2 and peroxisome proliferators-activated receptors- Results: PRDX6 and mPRDX6 were successfully expressed and purified. The results of efficacy study showed that the mutant mPRDX6, in which the phospholipaseA2 (PLA2) activity of PRDX6 was deleted by site directed mutation, had a better protective effect against the myocardial injury than PRDX6. CCK8 results showed that compared with that in ISO group, the proliferation activity of H9C2 cells was significantly enhanced ( Conclusion: mPRDX6 has a protective effect against the myocardial injury induced by ISO, and the mechanism may be related to its antioxidation. This study may provide a theoretical basis for the research and development of drugs used for the treatment of myocardial injury.
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