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Resveratrol inhibits rabies virus infection in N2a cells by activating the SIRT1/Nrf2/HO-1 pathway

Authors :
Qian Liu
Qing He
Xiaoyan Tao
Pengcheng Yu
Shuqing Liu
Yuan Xie
Wuyang Zhu
Source :
Heliyon, Vol 10, Iss 17, Pp e36494- (2024)
Publication Year :
2024
Publisher :
Elsevier, 2024.

Abstract

Rabies is a highly lethal infectious disease with no existing treatment available, thus investigating effective antiviral compounds to control rabies virus (RABV) infection is of utmost importance. Resveratrol is a natural phenolic compound that, as a phytoalexin, exhibits several biological activities, including antiviral activity. In this study, we evaluated the inhibitory effect of resveratrol on RABV infection and investigated its molecular antiviral mechanism. We found that resveratrol significantly inhibited RABV infection, including the phases of adsorption, replication, and release, and also directly inactivated RABV and inhibited its infectivity. However, resveratrol had no significant effect on RABV internalization. Resveratrol also reduced RABV-induced oxidative stress, specifically reactive oxygen species and malondialdehyde levels. Western blotting analysis revealed that resveratrol enhanced antioxidant signaling via the SIRT1/Nrf2/HO-1 pathway and inhibited viral replication. Viral infection was enhanced after SIRT1 knockdown, which inhibited the SIRT1/Nrf2/HO-1 antioxidant signaling pathway, suggesting that this pathway plays an important role in RABV replication. Overall, resveratrol prevented the adsorption, replication, and release of RABV and directly inactivated RABV, but failed to inhibit RABV internalization. Furthermore, resveratrol activated the SIRT1/Nrf2/HO-1 pathway to inhibit RABV replication and suppressed RABV-induced oxidative stress. These findings highlight the therapeutic potential of resveratrol for fighting RABV infections.

Details

Language :
English
ISSN :
24058440
Volume :
10
Issue :
17
Database :
Directory of Open Access Journals
Journal :
Heliyon
Publication Type :
Academic Journal
Accession number :
edsdoj.7965fce1214e4c479f0530ee348df5b1
Document Type :
article
Full Text :
https://doi.org/10.1016/j.heliyon.2024.e36494