ArticleActa cirurgica brasileira2024
Protective function of albiflorin against ferroptosis in exhaustive exerciseinduced myocardial injury via the AKT/Nrf2/HO-1 signaling.
Article in Acta cirurgica brasileira, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Enhanced terpenoid synthesis in Alternaria alstroemeriae PPL7 via co-fermentation with Paeonia lactiflora roots: integrated metabolomic and transcriptomic analysis.Archives of microbiology · 2026Article
- Pharmacology-Driven Dissection of Core Component Sets of Xuefu Zhuyu Decoction in Blood Stasis-Related Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Albiflorin Relieves Intervertebral Disc Degeneration Through Inhibiting Nucleus Pulposus Cell via the p38 MAPK/NF-κB Pathway.Immunity, inflammation and disease · 2026Article
- Albiflorin, a Monoterpene Glycoside, Protects Myoblasts against Hydrogen Peroxide-Induced Apoptosis by Activating the Nrf2/HO-1 Axis.Biomolecules & therapeutics · 2025Article
- Network pharmacological analysis, Mendelian randomization analysis and animal experimental reveal the mechanism of Wenxin Granules in inhibiting heart failure after myocardial infarction: apoptosis and inflammation.Frontiers in cardiovascular medicine · 2025Article
- Revisiting the Benefits of Exercise for Alzheimer's Disease through the Lens of Ferroptosis: A New Perspective.Aging and disease · 2024Review
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Authors and funding
2 authors.
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No grant is acknowledged in the PubMed record.
Abstract
purposeIt has been reported that exhaustive exercise (EE) causes myocyte injury, and eventually damages the function of the myocardia. Albiflorin (AF) has anti-inflammatory, antioxidant, and anti-apoptosis effects. In this study, we determined whether AF could mitigate the EE-induced myocardial injury and research the potential mechanisms.
methodsThe rat model of EE was built by forced treadmill running method. Rats were intraperitoneally injected with AF before EE once daily for one week. The relative factors levels were examined by commercial kits. The apoptosis was appraised using a TdT-mediated dUTP nick end labeling assay kit. The ACSL4, GPX4, Nrf2, pAKT/AKT, and HO-1 contents were assessed by western blot.
resultsAF lessened EE-induced cardiac myocytes ischemic/hypoxic injury and reduced the contents of myocardial injury biomarkers in the serum. AF lessened EE-induced cardiac myocyte apoptosis, inflammatory response, oxidative stress, and ferroptosis in myocardial tissues. However, the influences of AF were overturned by the co-treatment of AF and LY294002. AF activated the AKT/Nrf2/HO-1 signaling pathway in myocardial tissues in vivo.
conclusionsAF could curb cardiac myocytes ferroptosis, thus diminishing the EE-induced myocardial injury through activating the AKT/Nrf2/HO-1 cascade.
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