ArticleBritish journal of pharmacology2011
Scutellarin alleviates interstitial fibrosis and cardiac dysfunction of infarct rats by inhibiting TGFβ1 expression and activation of p38-MAPK and ERK1/2.
Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 104 citations in OpenAlex.
- Chinese Herbal Medicines for Diabetic Cardio-Cerebrovascular Diseases: Key Bioactive Metabolites and Action Mechanisms.Journal of nutrition and metabolism · 2026Review
- Liver-Targeted Scutellarin Nanoemulsion Alleviates Fibrosis with Ancillary Modulation of the Gut-Liver Microbiota.International journal of molecular sciences · 2025Article
- Scutellarin ameliorates ischemia/reperfusion-mediated endothelial dysfunction by upregulating cathepsin D expression to rescue autophagy-lysosomal function.Frontiers in pharmacology · 2025Article
- Review
- Article
- The Senescent Heart-"Age Doth Wither Its Infinite Variety".International journal of molecular sciences · 2024Review
- Sphingosylphosphorylcholine alleviates pressure overload-induced myocardial remodeling in mice via inhibiting CaM-JNK/p38 signaling pathway.Acta pharmacologica Sinica · 2024Article
- Scutellarin: pharmacological effects and therapeutic mechanisms in chronic diseases.Frontiers in pharmacology · 2024Review
- Promising Therapeutic Treatments for Cardiac Fibrosis: Herbal Plants and Their Extracts.Cardiology and therapy · 2023Review
- Supplementation with okra combined or not with exercise training is able to protect the heart of animals with metabolic syndrome.Scientific reports · 2023Article
- Effects of scutellarin on the mechanism of cardiovascular diseases: a review.Frontiers in pharmacology · 2023Review
- Scutellarin suppresses triple-negative breast cancer metastasis by inhibiting TNFα-induced vascular endothelial barrier breakdown.Acta pharmacologica Sinica · 2022Article
- Scutellarin ameliorates neonatal hypoxic-ischemic encephalopathy associated with GAP43-dependent signaling pathway.Chinese medicine · 2021Article
- Lefty1 Ameliorates Post-infarction Fibrosis by Suppressing p-Smad2 and p-ERK1/2 Signaling Pathways.Journal of cardiovascular translational research · 2021Article
- Therapeutic miR-21 Silencing Reduces Cardiac Fibrosis and Modulates Inflammatory Response in Chronic Chagas Disease.International journal of molecular sciences · 2021Article
- Scutellarin-induced A549 cell apoptosis depends on activation of the transforming growth factor-β1/smad2/ROS/caspase-3 pathway.Open life sciences · 2021Article
- Crocin attenuates isoprenaline-induced myocardial fibrosis by targeting TLR4/NF-κB signaling: connecting oxidative stress, inflammation, and apoptosis.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Anti-colorectal cancer effects of scutellarin revealed by genomic and proteomic analysis.Chinese medicine · 2020Article
- Long non-coding RNA cardiac hypertrophy-associated regulator governs cardiac hypertrophy via regulating miR-20b and the downstream PTEN/AKT pathway.Journal of cellular and molecular medicine · 2019Article
- MK5 haplodeficiency decreases collagen deposition and scar size during post-myocardial infarction wound repair.American journal of physiology. Heart and circulatory physiology · 2019Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeInterstitial fibrosis plays a causal role in the development of heart failure after chronic myocardial infarction (MI), and anti-fibrotic therapy represents a promising strategy to mitigate this pathological process. The purpose of this study was to investigate the effect of long-term administration of scutellarin (Scu) on cardiac interstitial fibrosis of myocardial infarct rats and the underlying mechanisms. EXPERIMENTAL APPROACH: Scu was administered to rats that were subjected to coronary artery ligation. Eight weeks later, its effects on cardiac fibrosis were assessed by examining cardiac function and histology. The number and collagen content of cultured cardiac fibroblasts exposed to angiotensin II (Ang II) were determined after the administration of Scu in vitro. Protein expression was detected by Western blot technique, and mRNA levels by quantitative reverse transcription-PCR. KEY
resultsThe echocardiographic and haemodynamic measurements showed that Scu improved the impaired cardiac function of infarct rats and decreased interstitial fibrosis. Scu inhibited the expression of FN1 and TGFβ1, but produced no effects on inflammatory cytokines (TNFα, IL-1β and IL-6) in the 8 week infarct hearts. Scu inhibited the proliferation and collagen production of cardiac fibroblasts (CFs) and the up-regulation of FN1 and TGFβ1 induced by Ang II. The enhanced phosphorylation of p38-MAPK and ERK1/2 in both infarct cardiac tissue and cultured CFs challenged by Ang II were suppressed by Scu. CONCLUSIONS AND IMPLICATIONS: Long-term administration of Scu improved the cardiac function of MI rats by inhibiting interstitial fibrosis, and the mechanisms may involve the suppression of pro-fibrotic cytokine TGFβ1 expression and inhibition of p38 MAPK and ERK1/2 phosphorylation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.