Biomol Ther.
2025 Mar;33(2):388-398. 10.4062/biomolther.2024.204.
Quercetin-3-Methyl Ether Induces Early Apoptosis to Overcome HRV1B Immune Evasion, Suppress Viral Replication, and Mitigate Inflammatory Pathogenesis
- Affiliations
-
- 1Department of Pharmacy, Kangwon National University, Chuncheon 24341, Republic of Korea
- 2Kangwon Institute of Inclusive Technology, Kangwon National University, Chuncheon 24341, Republic of Korea
- 3College of Pharmacy, Yeungnam University, Gyeongsan 38541, Republic of Korea
- 4Division of Acute Viral Diseases, Centers for Emerging Virus Research, National Institute of Health, Korea Disease Control and Prevention Agency, Cheongju 28159, Republic of Korea
- 5Division of Biomedical Convergence, College of Biomedical Science, Institue od Bioscience & Biotechnology, Kangwon National University, Chuncheon 24341, Republic of Korea
- 6Nucleic Acid Therapeutics Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju 28116, Republic of Korea
- 7Department of Biomolecular Science, KRIBB School of Bioscience, Korea University of Science and Technology (KUST), Daejeon 34113, Republic of Korea
- 8Department of Beauty Art, Youngsan University, 142 Bansong Beltway, Busan 48015, Republic of Korea
- KMID: 2565699
- DOI: http://doi.org/10.4062/biomolther.2024.204
Abstract
- Human rhinovirus (HRV) causes the common cold and exacerbates chronic respiratory diseases, such as asthma and chronic obstructive pulmonary disease. Despite its significant impact on public health, there are currently no approved vaccines or antiviral treatments for HRV infection. Apoptosis is the process through which cells eliminate themselves through the systematic activation of intrinsic death pathways in response to various stimuli. It plays an important role in viral infections and serves as a key immune defense mechanism in the interactions between viruses and the host. In the present study, we investigated the antiviral effects of quercetin-3-methyl ether, a flavonoid isolated from Serratula coronata, on human rhinovirus 1B (HRV1B). Quercetin-3-methyl ether significantly inhibited HRV1B replication in HeLa cells in a concentration-dependent manner, thereby reducing cytopathic effects and viral RNA levels. Time-course and time-of-addition analyses confirmed that quercetin-3-methyl ether exhibited antiviral activity during the early stages of viral infection, potentially targeting the replication and translation phases. Gene expression analysis using microarrays revealed that pro-apoptotic genes were upregulated in quercetin-3-methyl ether-treated cells, suggesting that quercetin-3-methyl ether enhances early apoptosis to counteract HRV1B-induced immune evasion. In vivo administration of quercetin-3-methyl ether to HRV1B-infected mice significantly reduced viral RNA levels and inflammatory cytokine production in the lung tissues. Our findings demonstrated the potential of quercetin-3-methyl ether as a novel antiviral agent against HRV1B, thereby providing a promising therapeutic strategy for the management of HRV1B infections and related complications.
- Full Text Links
-
- Actions
-
Cited
- CITED
-
- Close
- Share
-
- Similar articles
-
- Quercetin induces cell death by caspase-dependent and p38 MAPK pathway in EGFR mutant lung cancer cells
- Autophagy Inhibition Promotes Quercetin Induced Apoptosis in MG-63 Human Osteosarcoma cells
- Quercetin induces apoptosis and cell cycle arrest in triple-negative breast cancer cells through modulation of Foxo3a activity
- Anti-Human Rhinovirus 1B Activity of Dexamethasone viaGCR-Dependent Autophagy Activation
- Antiviral and Anti-Inflammatory Activities of Pochonin D, a Heat Shock Protein 90 Inhibitor, against Rhinovirus Infection
