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논문 기본 정보

자료유형
학술저널
저자정보
Ni Wang (Sun Yat-sen University) Junyan Yang (Chongqing Medical University) Ruijun Chen (The University of Hong Kong) Yunyun Liu (Sun Yat-sen University) Shunjie Liu (Sun Yat-sen University) Yining Pan (The University of Hong Kong) Qingfeng Lei (Sun Yat-sen University) Yuzhou Wang (Sun Yat-sen University) Lu He (Sun Yat-sen University) Youqiang Song (The University of Hong Kong) Zhong Li (Sun Yat-sen University)
저널정보
고려인삼학회 Journal of Ginseng Research Journal of Ginseng Research Vol.47 No.3
발행연도
2023.5
수록면
448 - 457 (10page)

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Background: Alzheimer’s disease (AD) is a common form of dementia, and impaired mitophagy is a hallmark of AD. Mitophagy is mitochondrial-specific autophagy. Ginsenosides from Ginseng involve in autophagy in cancer. Ginsenoside Rg1 (Rg1 hereafter), a single compound of Ginseng, has neuroprotective effects on AD. However, few studies have reported whether Rg1 can ameliorate AD pathology by regulating mitophagy.
Methods: Human SH-SY5Y cell and a 5XFAD mouse model were used to investigate the effects of Rg1. Rg1 (1μM) was added to β-amyloid oligomer (AβO)-induced or APPswe-overexpressed cell models for 24 hours. 5XFAD mouse models were intraperitoneally injected with Rg1 (10 ㎎/㎏/d) for 30 days. Expression levels of mitophagy-related markers were analyzed by western blot and immunofluorescent staining. Cognitive function was assessed by Morris water maze. Mitophagic events were observed using transmission electron microscopy, western blot, and immunofluorescent staining from mouse hippocampus. The activation of the PINK1/Parkin pathway was examined using an immunoprecipitation assay.
Results: Rg1 could restore mitophagy and ameliorate memory deficits in the AD cellular and/or mouse model through the PINK1-Parkin pathway. Moreover, Rg1 might induce microglial phagocytosis to reduce b-amyloid (Aβ) deposits in the hippocampus of AD mice.
Conclusion: Our studies demonstrate the neuroprotective mechanism of ginsenoside Rg1 in AD models. Rg1 induces PINK-Parkin mediated mitophagy and ameliorates memory deficits in 5XFAD mouse models.

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ABSTRACT
1. Introduction
2. Materials and methods
3. Results
4. Discussion
5. Conclusion
References

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