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논문 기본 정보

자료유형
학술저널
저자정보
Buyun Kim (Korea Institute of Oriental Medicine (KIOM)) Young Soo Kim (Korea Institute of Oriental Medicine (KIOM)) Wei Li (Korea Institute of Oriental Medicine (KIOM)) Eun-Bin Kwon (Korea Institute of Oriental Medicine (KIOM)) Hwan-Suck Chung (Korea Institute of Oriental Medicine (KIOM)) Younghoon Go (Korea Institute of Oriental Medicine (KIOM)) Jang- Gi Choi (Korea Institute of Oriental Medicine (KIOM))
저널정보
고려인삼학회 Journal of Ginseng Research Journal of Ginseng Research Vol.48 No.4
발행연도
2024.7
수록면
384 - 394 (11page)

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초록· 키워드

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Background: Herpes simplex virus type 1 (HSV-1), known to latently infect the host’s trigeminal ganglion, can lead to severe herpes encephalitis or asymptomatic infection, potentially contributing to neurodegenerative diseases like Alzheimer’s. The virus generates reactive oxygen species (ROS) that significantly impact viral replication and induce chronic inflammation through NF-κB activation. Nuclear factor E2-related factor 2 (Nrf2), an oxidative stress regulator, can prevent and treat HSV-1 infection by activating the passive defense response in the early stages of infection.
Methods and results: Our study investigated the antiviral effects of ginsenoside Rg5, an Nrf2 activator, on HSV-1 replication and several host cell signaling pathways. We found that HSV-1 infection inhibited Nrf2 activity in host cells, induced ROS/NF-κB signaling, and triggered inflammatory cytokines. However, treatment with ginsenoside Rg5 inhibited ROS/NF-κB signaling and reduced inflammatory cytokines through NRF2 induction. Interestingly, the Nrf2 inhibitor ML385 suppressed the expression of NAD(P)H quinone oxidoreductase 1(NQO1) and enhanced the expression of KEAP1 in HSV-1 infected cells. This led to the reversal of VP16 expression inhibition, a protein factor associated with HSV-1 infection, thereby promoting HSV-1 replication.
Conclusion: These findings suggest for the first time that ginsenoside Rg5 may serve as an antiviral against HSV-1 infection and could be a novel therapeutic agent for HSV-1-induced neuroinflammation.

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ABSTRACT
1. Introduction
2. Material and methods
3. Results
4. Discussion
5. Conclusions
References

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