ArticleBMC complementary and alternative medicine2014
Effects of stachydrine on norepinephrine-induced neonatal rat cardiac myocytes hypertrophy and intracellular calcium transients.
Article in BMC complementary and alternative medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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13 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Stachydrine: A Systematic Review of Its Multi-Targeted Therapeutic Potential in Cardiovascular, Oncology, Renal, Gynecological, and Inflammatory Disorders.Drug design, development and therapy · 2026Pooled it
- Stachydrine ameliorates hypoxia reoxygenation injury of cardiomyocyte via enhancing SIRT1-Nrf2 pathway.Journal of cardiothoracic surgery · 2023Article
- Stachydrine, a Bioactive Equilibrist for Synephrine, Identified from FourMolecules (Basel, Switzerland) · 2023Article
- Stachydrine alleviates lipid-induced skeletal muscle insulin resistance via AMPK/HO-1-mediated suppression of inflammation and endoplasmic reticulum stress.Journal of endocrinological investigation · 2022Article
- Stachydrine hydrochloride ameliorates cardiac hypertrophy through CaMKII/HDAC4/MEF2C signal pathway.American journal of translational research · 2022Article
- Therapeutic Effects of Traditional Chinese Medicine on Cardiovascular Diseases: the Central Role of Calcium Signaling.Frontiers in pharmacology · 2021Review
- Schisandrin Protects against Norepinephrine-Induced Myocardial Hypertrophic Injury by Inhibiting the JAK2/STAT3 Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Stachytine Hydrochloride Improves Cardiac Function in Mice with ISO-Induced Heart Failure by Inhibiting the α-1,6-Fucosylation on N-Glycosylation of β1AR.Frontiers in pharmacology · 2021Article
- Stachydrine Ameliorates Cardiac Fibrosis Through Inhibition of Angiotensin II/Transformation Growth Factor β1 Fibrogenic Axis.Frontiers in pharmacology · 2019Article
- Article
- Benificial Effect of Stachydrine on the Traumatic Brain Injury Induced Neurodegeneration by Attenuating the Expressions of Akt/mTOR/PI3K and TLR4/NFκ-B Pathway.Translational neuroscience · 2018Article
- Chronic hypoxia alters fetal cerebrovascular responses to endothelin-1.American journal of physiology. Cell physiology · 2017Article
- Stachydrine ameliorates pressure overload-induced diastolic heart failure by suppressing myocardial fibrosis.American journal of translational research · 2017Article
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7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLeonurus heterophyllus sweet has been suggested to have cardioprotective effects against heart diseases, including ischemic diseases and ventricular remodeling. However, the active ingredients of the herb and the underlying mechanisms are poorly understood. The aim of the present study was to investigate the effects of stachydrine (STA), a major constituent of Leonurus heterophyllus sweet, on norepinephrine (NE) induced hypertrophy and the changes of calcium transients in neonatal rat cardiomyocytes.
methodsVentricular myocytes from 1-day-old Wistar rats were isolated and cultured in DMEM/F12 with 1 μmol/L norepinephrine in the presence or absence of 10 μmol/L STA for 72 h. Cardiomyocytes hypertrophy was evaluated by cell surface area, total protein/DNA content, β/α-MHC mRNA ratio. While calcium handling function was evaluated by Ca2+-transient amplitude and decay, SERCA2a activity and expression, PLN expression and phosphorylation. β1-adrenergic receptor system activation was evaluated by the content of cAMP and the activation of PKA.
resultsNE treatment increases the cell surface area, protein synthesis, the expression level of β-MHC and β/α-MHC ratio. These effects were attenuated by STA. NE-induced hypertrophy was associated with increased Ca2+-transient amplitude, accelerated decay of the Ca2+-transient, increased phospholamban expression, hyper-phosphorylation at both the serine-16 and threonine-17 residues, increased intracellular cAMP level, and PKA overactivation. All of which were significantly inhibited by STA.
conclusionThese data suggest that STA attenuates norepinephrine-induced cardiomyocyte hypertrophy and has potential protective effects against β-adrenergic receptor induced Ca2+ mishandling.
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