ArticleOxidative medicine and cellular longevity2015
The Protective Effects of Salidroside from Exhaustive Exercise-Induced Heart Injury by Enhancing the PGC-1 α -NRF1/NRF2 Pathway and Mitochondrial Respiratory Function in Rats.
Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 81 citations in OpenAlex.
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- Salidroside alleviates simulated microgravity-induced bone loss by activating the Nrf2/HO-1 pathway.Journal of orthopaedic surgery and research · 2024Article
- Potential Applications of Mitochondrial Therapy with a Focus on Parkinson's Disease and Mitochondrial Transplantation.Advanced pharmaceutical bulletin · 2024Review
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- Dehydroeburicoic Acid, a Dual Inhibitor against Oxidative Stress in Alcoholic Liver Disease.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Novel Insights into Floral Thermogenesis: In Vivo Analyses of Mitochondrial Dynamics inInternational journal of molecular sciences · 2022Article
- Review
- Exercise and mitochondrial mechanisms in patients with sarcopenia.Frontiers in physiology · 2022Review
- Establishment and identification of an animal model of long-term exercise-induced fatigue.Frontiers in endocrinology · 2022Review
- Novel insights into exhaustive exercise-induced myocardial injury: Focusing on mitochondrial quality control.Frontiers in cardiovascular medicine · 2022Review
- The role of Nrf2 in periodontal disease by regulating lipid peroxidation, inflammation and apoptosis.Frontiers in endocrinology · 2022Review
- Optimization of different intensities of exercise preconditioning in protecting exhausted exercise induced heart injury in rats.Sports medicine and health science · 2021Article
- Comparison of myocardial ischemic/hypoxic staining techniques for evaluating the alleviation of exhaustive exercise-induced myocardial injury by exercise preconditioning.Journal of molecular histology · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo test the hypothesis that salidroside (SAL) can protect heart from exhaustive exercise-induced injury by enhancing mitochondrial respiratory function and mitochondrial biogenesis key signaling pathway PGC-1α-NRF1/NRF2 in rats.
methodsMale Sprague-Dawley rats were divided into 4 groups: sedentary (C), exhaustive exercise (EE), low-dose SAL (LS), and high-dose SAL (HS). After one-time exhaustive swimming exercise, we measured the changes in cardiomyocyte ultrastructure and cardiac marker enzymes and mitochondrial electron transport system (ETS) complexes activities in situ. We also measured mitochondrial biogenesis master regulator PGC-1α and its downstream transcription factors, NRF1 and NRF2, expression at gene and protein levels.
resultsCompared to C group, the EE group showed marked myocardium ultrastructure injury and decrease of mitochondrial respiratory function (P < 0.05) and protein levels of PGC-1α, NRF1, and NRF2 (P < 0.05) but a significant increase of PGC-1α, NRF1, and NRF2 genes levels (P < 0.05); compared to EE group, SAL ameliorated myocardium injury, increased mitochondrial respiratory function (P < 0.05), and elevated both gene and protein levels of PGC-1α, NRF-1, and NRF-2.
conclusionSalidroside can protect the heart from exhaustive exercise-induced injury. It might act by improving myocardial mitochondrial respiratory function by stimulating the expression of PGC-1α-NRF1/NRF2 pathway.
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