ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2019
Emodin protects H9c2 cells from hypoxia-induced injury by up-regulating miR-138 expression.
Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Cardioprotective Effects ofLife (Basel, Switzerland) · 2026Review
- Emodin influences pyroptosis-related Caspase 1-GSDMD axis alleviated cerebral ischemia-reperfusion injury in rats.Scientific reports · 2025Article
- Therapeutic Implications of Traditional Chinese Medicine in Clinically Relevant Diseases: Perspectives From microRNA-Modulated Apoptotic Signaling.Drug design, development and therapy · 2025Review
- Navigating the Landscape of Coronary Microvascular Research: Trends, Triumphs, and Challenges Ahead.Reviews in cardiovascular medicine · 2024Review
- Article
- Recent advances of traditional Chinese medicine against cardiovascular disease: overview and potential mechanisms.Frontiers in endocrinology · 2024Review
- Emodin improves the cardiac function in the rats with chronic heart failure through regulation of the miR-26b-5p/PTEN pathway.Archives of medical science : AMS · 2024Article
- MLK3 silence suppressed osteogenic differentiation and delayed bone formation via influencing the bone metabolism and disturbing MAPK signaling.Journal of orthopaedic translation · 2023Article
- Emodin in cardiovascular disease: The role and therapeutic potential.Frontiers in pharmacology · 2022Review
- Uncovering the Effect and Mechanism ofFrontiers in pharmacology · 2022Article
- Effects of emodin, a plant-derived anthraquinone, on TGF-β1-induced cardiac fibroblast activation and function.Journal of cellular physiology · 2021Article
- Hyperoside protects cardiomyocytes against hypoxia‑induced injury via upregulation of microRNA‑138.Molecular medicine reports · 2021Article
- Up-regulating microRNA-138-5p enhances the protective role of dexmedetomidine on myocardial ischemia-reperfusion injury mice via down-regulating Ltb4r1.Cell cycle (Georgetown, Tex.) · 2021Article
- Pyroptosis and ferroptosis induced by mixed lineage kinase 3 (MLK3) signaling in cardiomyocytes are essential for myocardial fibrosis in response to pressure overload.Cell death & disease · 2020Article
- Emodin and emodin-rich rhubarb inhibits histone deacetylase (HDAC) activity and cardiac myocyte hypertrophy.The Journal of nutritional biochemistry · 2020Article
- Molecular Mechanisms of Action of Emodin: As an Anti-Cardiovascular Disease Drug.Frontiers in pharmacology · 2020Review
- CLEC3B protects H9c2 cardiomyocytes from apoptosis caused by hypoxia via the PI3K/Akt pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020Article
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6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Myocardial infarction (MI) is a common presentation for ischemic heart disease, which is a leading cause of death. Emodin is a Chinese herbal anthraquinone used in several diseases. However, the effect of emodin in hypoxia-induced injury in cardiomyocytes has not been clearly elucidated. Our study aimed to clarify the functions of emodin in hypoxia-induced injury in rat cardiomyocytes H9c2 and explore the underlying mechanism. The effects of emodin on cell viability and apoptosis were analyzed by the Cell counting kit-8 assay and flow cytometry assay, respectively. The cell proliferation- and cell apoptosis-related proteins were detected by western blot. qRT-PCR was used to determine the relative expression of miR-138. Cell transfection was performed to alter miR-138 and MLK3 expression. miR-138 target was performed by dual luciferase activity assay. Sirt1/AKT and Wnt/β-catenin pathways-related factors phosphorylation were analyzed by western blot. Emodin inhibited hypoxia-induced injury in H9c2 cells by promoting cell viability and reducing cell apoptosis. miR-138 was down-regulated by hypoxia treatment but up-regulated by emodin. Up-regulation of miR-138 alleviated hypoxia-induced cell injury. Down-regulation of miR-138 attenuated the growth-promoting effect of emodin on hypoxia-induced injury, whereas up-regulation of miR-138 enhanced the growth-promoting effects of emodin. The underlying mechanism might be by inactivating Sirt1/AKT and Wnt/β-catenin pathways. MLK3 was negatively regulated by miR-138 expression and inactivated Sirt1/AKT and Wnt/β-catenin pathways. Emodin alleviated hypoxia-induced injury in H9c2 cells via up-regulation of miR-138 modulated by MLK3, as well as by activating Sirt1/AKT and Wnt/β-catenin pathways.
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