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Updated: Jun 18, 2026
Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons
Published on: August 23, 2016
Fisetin limits Chikungunya virus-induced apoptosis hallmarks in hepatocellular carcinoma cells
Rafidah Lani1, Pouya Hassandarvish2, Sazaly AbuBakar3
1Department of Medical Microbiology, Faculty of Medicine, Universiti Malaya, Kuala Lumpur, 50603, Malaysia. rafidahl@um.edu.my.
Abstract:
The study investigated the protective effects of fisetin on chikungunya virus (CHIKV)-induced apoptosis hallmarks in Huh7 cells. Fisetin significantly reduced CHIKV RNA levels and viral infectivity, outperforming Z-VAD-FMK and cisplatin. At 30 µM, fisetin markedly decreased (by > 90%) the number of infectious viral particles at 24 and 48 h post-infection (hpi). Fisetin also hindered CHIKV-induced DNA fragmentation, with the lowest levels observed in CHIKV-infected cells treated with fisetin compared to other treatments. Immunoblot analysis revealed that fisetin inhibited caspase-mediated PARP cleavage and significantly reduced cleaved PARP levels, indicating decreased apoptosis. Additionally, fisetin diminished the expression of cleaved caspase-3 and HSP-27 proteins, while restoring HIF-1α protein levels, suggesting a protective role against CHIKV-induced apoptosis. The study highlights the potential of fisetin as an effective antiviral agent against CHIKV through the modulation of apoptosis and oxidative stress pathways. These findings underscore the therapeutic promise of fisetin for treating CHIKV-induced apoptosis and warrant further investigation to explore its clinical applications and optimize its use in antiviral therapy.
Insights
Fisetin effectively combats chikungunya virus (CHIKV) by reducing viral load and inhibiting apoptosis. This natural compound shows promise as an antiviral therapy for CHIKV infections.
Area of Science:
- Virology
- Cell Biology
- Pharmacology
Background:
- Chikungunya virus (CHIKV) infection poses a significant global health threat.
- CHIKV infection induces cellular apoptosis, contributing to disease pathogenesis.
- Limited effective antiviral treatments are currently available for CHIKV.
Purpose of the Study:
- To investigate the protective effects of fisetin against CHIKV-induced apoptosis in vitro.
- To evaluate fisetin's efficacy in reducing viral replication and infectivity.
- To elucidate the molecular mechanisms underlying fisetin's antiviral and anti-apoptotic actions.
Main Methods:
- Huh7 cells were infected with CHIKV and treated with varying concentrations of fisetin.
- Viral RNA levels and infectious viral particle production were quantified.
- Apoptosis hallmarks, including DNA fragmentation, PARP cleavage, and caspase-3 activation, were assessed via immunoblot analysis.
- Expression levels of HSP-27 and HIF-1α were also analyzed.
Main Results:
- Fisetin significantly reduced CHIKV RNA levels and viral infectivity, outperforming Z-VAD-FMK and cisplatin.
- At 30 µM, fisetin decreased infectious viral particles by over 90% at 24 and 48 hours post-infection.
- Fisetin inhibited CHIKV-induced DNA fragmentation, PARP cleavage, and cleaved caspase-3 expression.
- Fisetin treatment restored HIF-1α protein levels and diminished HSP-27 expression.
Conclusions:
- Fisetin demonstrates potent antiviral activity against CHIKV by mitigating apoptosis and viral replication.
- Fisetin modulates key apoptotic and oxidative stress pathways, offering a protective effect.
- These findings highlight fisetin's therapeutic potential for CHIKV treatment and warrant further clinical investigation.
