ArticleFrontiers in pharmacology2017
Andrographolide Protects against Aortic Banding-Induced Experimental Cardiac Hypertrophy by Inhibiting MAPKs Signaling.
Article in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 38 citations in OpenAlex.
- Cardiac function of colorectal cancer mice is remotely controlled by gut microbiota: regulating serum metabolites and myocardial cytokines.Animal microbiome · 2025Article
- Natural terpenoids with therapeutic potential against pulmonary arterial hypertension.Frontiers in pharmacology · 2025Review
- Enhanced prevention on postoperative atrial fibrillation by using anti-inflammatory biodegradable drug patch.Regenerative biomaterials · 2025Article
- Andrographolide contributes to the attenuation of cardiac hypertrophy by suppressing endoplasmic reticulum stress.Pharmaceutical biology · 2023Article
- Promising Therapeutic Treatments for Cardiac Fibrosis: Herbal Plants and Their Extracts.Cardiology and therapy · 2023Review
- Andrographolide protects against atrial fibrillation by alleviating oxidative stress injury and promoting impaired mitochondrial bioenergetics.Journal of Zhejiang University. Science. B · 2023Article
- Metallothionein-2A Protects Cardiomyocytes from Hypoxia/reper-Fusion through Inhibiting p38.Cell biochemistry and biophysics · 2023Article
- Andrographolide Protects Against Adverse Cardiac Remodeling After Myocardial Infarction through Enhancing Nrf2 Signaling Pathway.International journal of biological sciences · 2020Article
- Cordycepin ameliorates cardiac hypertrophy via activating the AMPKα pathway.Journal of cellular and molecular medicine · 2019Article
- Bcl6 Suppresses Cardiac Fibroblast Activation and Function via Directly Binding to Smad4.Current medical science · 2019Article
- Regulatory Mechanisms of the NLRP3 Inflammasome, a Novel Immune-Inflammatory Marker in Cardiovascular Diseases.Frontiers in immunology · 2019Review
- Pterostilbene Attenuates Fructose-Induced Myocardial Fibrosis by Inhibiting ROS-Driven Pitx2c/miR-15b Pathway.Oxidative medicine and cellular longevity · 2019Article
- Andrographolide Protects against HG-Induced Inflammation, Apoptosis, Migration, and Impairment of Angiogenesis via PI3K/AKT-eNOS Signalling in HUVECs.Mediators of inflammation · 2019Article
- NLRP3 deficiency accelerates pressure overload-induced cardiac remodeling via increased TLR4 expression.Journal of molecular medicine (Berlin, Germany) · 2018Article
- miR-133: A Suppressor of Cardiac Remodeling?Frontiers in pharmacology · 2018Review
- Andrographolide Mitigates DOCA-Salt-Induced Cardiac Hypertrophy by Regulating Calcium-Handling Genes.Journal of pharmacy & bioallied sciencesArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite therapeutic advances, heart failure-related mortality rates remain high. Therefore, understanding the pathophysiological mechanisms involved in the remodeling process is crucial for the development of new therapeutic strategies. Andrographolide (Andr), a botanical compound, has potent cardio-protective effects due to its ability to inhibit mitogen-activated protein kinases (MAPKs). Andr has also been shown to inhibit inflammation and apoptosis, which are factors related to cardiac hypertrophy. Our aim was to evaluate the effects of Andr on cardiac hypertrophy and MAPKs activation. Thus, mice were subjected to aortic banding (AB) with/without Andr administration (25 mg/kg/day, orally). Cardiac function was accessed by echocardiography and hemodynamic parameters. Our results showed that Andr administration for 7 weeks decreased cardiac dysfunction and attenuated cardiac hypertrophy and fibrosis in AB mice. Andr treatment induced a strong reduction in the transcription of both hypertrophy (ANP, BNP, and β-MHC) and fibrosis related genes (collagen I, collagen III, CTGF, and TGFβ). In addition, cardiomyocytes treated with Andr showed a reduced hypertrophic response to angiotensin II. Andr significantly inhibited MAPKs activation in both mouse hearts and cardiomyocytes. Treatment with a combination of MAPKs activators abolished the protective effects of Andr in cardiomyocytes. Furthermore, we found that Andr also inhibited the activation of cardiac fibroblasts via the MAPKs pathway, which was confirmed by the application of MAPKs inhibitors. In conclusion, Andr was found to confer a protective effect against experimental cardiac hypertrophy in mice, suggesting its potential as a novel therapeutic drug for pathological cardiac hypertrophy.
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