ArticleArchives of medical science : AMS2024
Emodin improves the cardiac function in the rats with chronic heart failure through regulation of the miR-26b-5p/PTEN pathway.
Article in Archives of medical science : AMS, 2024. 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.
- Prognostic value of miR-26b-5p in prostate cancer and its regulatory effect on tumor progression.World journal of surgical oncology · 2026Article
- The pathophysiological role of MiRNAs in heart failure.Frontiers in cardiovascular medicine · 2026Review
- Exploring the Therapeutic Potential of Natural Compounds and Plant Extracts in Human Health.Biomolecules · 2025Article
- Rhubarb: Traditional Uses, Phytochemistry, Multiomics-Based Novel Pharmacological and Toxicological Mechanisms.Drug design, development and therapy · 2025Review
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Authors and funding
5 authors.
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Abstract
Introduction: Chronic heart failure (CHF) is a leading cause of deaths induced by cardiovascular disease. This study aimed to investigate the protective effects of emodin in CHF rats and explore the related mechanisms. Material and methods: A total of 56 Wistar rats were used to construct CHF model using the coronary artery ligation. The effects of emodin on cardiac function and inflammation were analyzed in the CHF rats. Expression of miR-26b-5p in the CHF model before and after emodin treatment was estimated by quantitative real-time polymerase chain reaction. The effects of miR-26b-5p on cardiac function and inflammation were also assessed, and its target gene was predicted and confirmed in rat cardiomyocyte H9c2. Results: Emodin treatment could significant improve the cardiac function and inflammation evidenced by the increased increased ejection fraction (EF), fractional shortening (FS), left ventricular systolic pressure (LVSP) and maximum of the first differentiation of left ventricular pressure (+LV dP/dt Conclusions: All the results indicated that emodin serves a protective role in CHF via regulation of the miR-26b-5p/PTEN pathway. Emodin may be an effective therapeutic agent for CHF treatment.
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