ArticleMolecular medicine reports2017
Effect of hyperoside on the apoptosis of A549 human non‑small cell lung cancer cells and the underlying mechanism.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Fraction-Dependent Polyphenolic Profile and Biological Activities ofAntioxidants (Basel, Switzerland) · 2026Article
- Mechanistic evaluation of hyperoside against non-small cell lung cancer: a combined approach of network pharmacology and in vitro experimental validation.Discover oncology · 2025Article
- LC-HRMS/MS-Guided Profiling and Biological Evaluation ofMolecules (Basel, Switzerland) · 2025Article
- An Overview of the Bioactivity of Spontaneous Medicinal Plants Suitable for the Improvement of Lung Cancer Therapies.Pharmaceutics · 2025Review
- Viability and Radiosensitivity of Human Tumor Cells from Breast and Colon Are Influenced byInternational journal of molecular sciences · 2025Article
- The multiple biological activities of hyperoside: from molecular mechanisms to therapeutic perspectives in neoplastic and non-neoplastic diseases.Frontiers in pharmacology · 2025Review
- Effects of Strawberry Tree (Toxics · 2024Article
- Quercetin Derivatives as Potential Therapeutic Agents: An Updated Perspective on the Treatment of Nicotine-Induced Non-Small Cell Lung Cancer.International journal of molecular sciences · 2023Review
- Evaluation of cytotoxic and apoptotic effects of the extracts and phenolic compounds ofSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023Article
- Potential Implications of Hyperoside on Oxidative Stress-Induced Human Diseases: A Comprehensive Review.Journal of inflammation research · 2023Review
- Hypericum Genus as a Natural Source for Biologically Active Compounds.Plants (Basel, Switzerland) · 2022Review
- Review
- Bioactive components, pharmacological effects, and drug development of traditional herbal medicineFrontiers in nutrition · 2022Review
- Antitumor Effect of Hyperoside Loaded in Charge Reversed and Mitochondria-Targeted Liposomes.International journal of nanomedicine · 2021Article
- Hyperoside Attenuates Bleomycin-Induced Pulmonary Fibrosis Development in Mice.Frontiers in pharmacology · 2020Article
- Hyperoside Induces Breast Cancer Cells Apoptosis via ROS-Mediated NF-κB Signaling Pathway.International journal of molecular sciences · 2019Article
- Effect of hyperoside on cervical cancer cells and transcriptome analysis of differentially expressed genes.Cancer cell international · 2019Article
- Apoptotic Pathway as the Therapeutic Target for Anticancer Traditional Chinese Medicines.Frontiers in pharmacology · 2019Review
- Effect of Total Flavones from Cuscuta Chinensis on Anti-Abortion via the MAPK Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperoside (HY) is a major pharmacologically active component from Prunella vulgaris L. and Hypericum perforatum. The present study aimed to determine the anticancer effect of HY and determine the underlying mechanisms involved. Human A549 cells were treated with HY (10, 50 and 100 µM), and cell viability was detected by an MTT assay. Cell apoptosis and mitochondrial membrane potential were determined by flow cytometry. Western blot analysis was used to identify the expression of apoptosis‑associated proteins and phosphorylation of MAPK. The present study demonstrated that HY significantly inhibited the viability of A549 cells in a time‑ and dose‑dependent manner, and enhanced the percentage of apoptotic cells. HY also significantly increased the protein phosphorylation of p38 mitogen‑activated protein kinase (MAPK) and c‑Jun N‑terminal kinase (JNK), disrupted mitochondrial membrane penetrability, and triggered the release of mitochondrial cytochrome c and apoptosis‑inducing factor into the cytosol. Treatment with HY also activated the expression of caspase‑9 and caspase‑3. These results suggested that HY‑induced apoptosis was associated with activation of the p38 MAPK‑ and JNK‑induced mitochondrial death pathway. HY may offer potential for clinical applications in treating human non‑small cell lung cancer and improving cancer chemotherapy.
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Registered trials
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.