ArticleOxidative medicine and cellular longevity2018
Aucubin Protects against Myocardial Infarction-Induced Cardiac Remodeling via nNOS/NO-Regulated Oxidative Stress.
Article in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- Iridoids as Multi-target Neuroprotective Agents for Ischemic Stroke: Mechanisms and Therapeutic Potential.Mini reviews in medicinal chemistry · 2026Review
- TRIM55 Aggravates Cardiomyocyte Apoptosis After Myocardial Infarction via Modulation of the Nrf2/HO-1 Pathway.JACC. Basic to translational science · 2024Article
- Aucubin promotes activation of AMPK and alleviates cerebral ischemia/reperfusion injury in rats.Cell stress & chaperones · 2023Article
- Targeting oxidative stress as a preventive and therapeutic approach for cardiovascular disease.Journal of translational medicine · 2023Review
- Characteristics, Isolation Methods, and Biological Properties of Aucubin.Molecules (Basel, Switzerland) · 2023Review
- Aucubin Exerts Neuroprotection against Forebrain Ischemia and Reperfusion Injury in Gerbils through Antioxidative and Neurotrophic Effects.Antioxidants (Basel, Switzerland) · 2023Article
- Identification ofFrontiers in microbiology · 2023Article
- Aucubin protects against retinal ganglion cell injury in diabetic rats via inhibition of the p38MAPK pathway.American journal of translational research · 2023Article
- Research progress on the protective effects of aucubin in neurological diseases.Pharmaceutical biology · 2022Review
- Acacetin alleviates myocardial ischaemia/reperfusion injury by inhibiting oxidative stress and apoptosis via the Nrf-2/HO-1 pathway.Pharmaceutical biology · 2022Article
- Beneficial effects of Aucubin on restoration of rabbits with cartilage defect.Cell and tissue banking · 2022Article
- Protection of toll-like receptor 9 against lipopolysaccharide-induced inflammation and oxidative stress of pulmonary epithelial cells via MyD88-mediated pathways.Physiological research · 2022Article
- The histone demthylase KDM3A protects the myocardium from ischemia/reperfusion injury via promotion of ETS1 expression.Communications biology · 2022Article
- Mechanism of tonifying-kidney Chinese herbal medicine in the treatment of chronic heart failure.Frontiers in cardiovascular medicine · 2022Review
- Aucubin Impeded Preosteoclast Fusion and Enhanced CD31Stem cells international · 2022Article
- Regulation of the PTEN/PI3K/AKT pathway in RCC using the active compounds of natural productsMolecular medicine reports · 2021Article
- Phosphoproteomic response of cardiac endothelial cells to ischemia and ultrasound.Biochimica et biophysica acta. Proteins and proteomics · 2021Article
- Traditional application and modern pharmacological research of Eucommia ulmoides Oliv.Chinese medicine · 2021Review
- Abnormal Mitochondria-Endoplasmic Reticulum Communication Promotes Myocardial Infarction.Frontiers in physiology · 2021Article
- Role of Muscle-Specific Histone Methyltransferase (Smyd1) in Exercise-Induced Cardioprotection against Pathological Remodeling after Myocardial Infarction.International journal of molecular sciences · 2020Article
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Authors and funding
9 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Whether aucubin could protect myocardial infarction- (MI-) induced cardiac remodeling is not clear. In this study, in a mouse model, cardiac remodeling was induced by left anterior descending coronary artery ligation surgery. Mice were intraperitoneally injected with aucubin (10 mg/kg) 3 days post-MI. Two weeks post-MI, mice in the aucubin treatment group showed decreased mortality, decreased infarct size, and improved cardiac function. Aucubin also decreased cardiac remodeling post-MI. Consistently, aucubin protected cardiomyocytes against hypoxic injury in vitro. Mechanistically, we found that aucubin inhibited the ASK1/JNK signaling. These effects were abolished by the JNK activator. Moreover, we found that the oxidative stress was attenuated in both in vivo aucubin-treated mice heart and in vitro-treated cardiomyocytes, which caused decreased thioredoxin (Trx) consumption, leading to ASK1 forming the inactive complex with Trx. Aucubin increased nNOS-derived NO production in vivo and vitro. The protective effects of aucubin were reversed by the NOS inhibitors L-NAME and L-VINO in vitro. Furthermore, nNOS knockout mice also reversed the protective effects of aucubin on cardiac remodeling. Taken together, aucubin protects against cardiac remodeling post-MI through activation of the nNOS/NO pathway, which subsequently attenuates the ROS production, increases Trx preservation, and leads to inhibition of the ASK1/JNK pathway.
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