Korean Red Ginseng Inhibits Amyloid-β-Induced Apoptosis and Nucling Expression in Human Neuronal Cells

Choi, Suyun; Lim, Joo Weon; Kim, Hye Young

doi:10.1159/000505592

Cited by 10 publications

(7 citation statements)

References 38 publications

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“…Thus, Aβ 25-35 was chosen for this experiment. The doses of Aβ 25-35 in our study were used according to relevant studies [ 36 , 37 ]. We firstly applied 5, 10, 20 or 50 μmol/L of Aβ 25-35 to test the neurotoxicity of Aβ 25-35 in the PC 12 cells.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effects of donepezil against Aβ25-35-induced neurotoxicity

Gao

Che

et al. 2022

Eur J Med Res

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Purpose The purpose of this study was to investigate the neuroprotective effect of donepezil against β-amyloid25-35 (Aβ25-35)-induced neurotoxicity and the possible mechanism. Methods PC12 cells were conventionally cultured. Serial concentrations of Aβ25-35 and donepezil (0, 0.5, 1, 5, 10, 20 and 50 μmol/L) were added to the PC12 cells, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) staining was performed to detect the effects of these treatments on PC 12 viability. The PC 12 cells were pretreated with 1, 5, 10, 20 or 50 μmol/L donepezil two hours before 20 μmol/L Aβ25-35 was added to pretreatment groups A, B, C, D and E. Normal control group I and the 20 μmol/L Aβ25-35-treated group were selected. An MTT assay was used to detect PC12 cell viability, and the level of lactate dehydrogenase (LDH) was determined. PC12 cells were pretreated with 10 μmol/L GF109203X (a protein kinase C [PKC] antagonist) 30 min before 10 μmol/L donepezil was added to pretreatment group F, and normal control group II, the 10 μmol/L GF109203X-treated group and the 10 μmol/L donepezil-treated group were chosen. The expression of phosphorylation-PKC (P-PKC) and its major substrate phosphorylated myristoylated alanine-rich protein C kinase substrate (P-MARCKS) was measured by Western blotting. The effects of donepezil on the subcellular distribution of the PKCα and PKCε isoforms were detected by immunofluorescence staining. Results Treatment with Aβ25-35 (5, 10, 20 or 50 μmol/L) for 24 h significantly (P < 0.05) decreased PC 12 cell viability in a dose-dependent manner. Compared with the PC12 cells in the control group, those in the 20 μmol/L Aβ25-35-treated group exhibited lower viability but higher LDH release. Compared with the 20 μmol/L Aβ25–35-treated group, pretreatment groups B, C, D and E exhibited significantly (P < 0.05) increased cell viability but significantly (P < 0.05) decreased LDH release. Western blotting demonstrated that compared with control, 10 μmol/L donepezil promoted PKC and MARCKS phosphorylation and that the expression of P-PKC and P-MARCKS in pretreatment group F was significantly (P < 0.05) lower than that in the donepezil-treated group. Immunofluorescence staining revealed that the PKCα and PKCε isoforms were located mainly in the cytoplasm of PC12 control cells, whereas donepezil increased the expression of the PKCα and PKCε isoforms in the membrane fraction. The Western blot results showed that donepezil altered the subcellular distribution of the PKCα and PKCε isoforms by decreasing their expression in the cytosolic fraction but increasing their expression in the membrane fraction. Conclusion Donepezil can antagonize Aβ25–350-induced neurotoxicity in PC 12 cells, and PKC activation may account for the neuroprotective effect of donepezil.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective effects of donepezil against Aβ25-35-induced neurotoxicity

Gao

Che

et al. 2022

Eur J Med Res

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“…Korean red ginseng extract (KRG) has been studied as a multi-component drug for AD in the clinical phase II. In vitro experiments, KRG inhibited apoptosis by activating the PI3K/Akt signaling pathway, suppressed NF-κB expression and decreased mitochondrial membrane potential, and also restored mitochondrial respiration associated with ATP production ( Nguyen et al, 2015 ; Shin et al, 2019 ; Choi et al, 2020 ). In addition, in 5XFAD mice that expressed five familial AD mutations, it was further demonstrated that KRG could inhibit the occurrence of mitochondrial dysfunction by protecting the mitochondrial fusion and fission processes, thereby protecting AD mice ( Shin et al, 2019 ).…”

Section: Neuronal Degenerative Diseases and Herbal Medicinementioning

confidence: 98%

Regulation of mitochondrial dysfunction induced cell apoptosis is a potential therapeutic strategy for herbal medicine to treat neurodegenerative diseases

Duan

et al. 2022

Front. Pharmacol.

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Neurodegenerative disease is a progressive neurodegeneration caused by genetic and environmental factors. Alzheimer’s disease (AD), Parkinson’s disease (PD), and Huntington’s disease (HD) are the three most common neurodegenerative diseases clinically. Unfortunately, the incidence of neurodegenerative diseases is increasing year by year. However, the current available drugs have poor efficacy and large side effects, which brings a great burden to the patients and the society. Increasing evidence suggests that occurrence and development of the neurodegenerative diseases is closely related to the mitochondrial dysfunction, which can affect mitochondrial biogenesis, mitochondrial dynamics, as well as mitochondrial mitophagy. Through the disruption of mitochondrial homeostasis, nerve cells undergo varying degrees of apoptosis. Interestingly, it has been shown in recent years that the natural agents derived from herbal medicines are beneficial for prevention/treatment of neurodegenerative diseases via regulation of mitochondrial dysfunction. Therefore, in this review, we will focus on the potential therapeutic agents from herbal medicines for treating neurodegenerative diseases via suppressing apoptosis through regulation of mitochondrial dysfunction, in order to provide a foundation for the development of more candidate drugs for neurodegenerative diseases from herbal medicine.

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“…In this background, ginseng, a widely used traditional medicine for centuries, could be a new alternative in the treatment of AD. Ginseng has been reported to have protective effects via multiple brain pathways, including anti-oxidative, anti-inflammatory, and immunomodulatory properties ( Park et al, 2013 ; Hossen et al, 2017 ), and some preclinical studies have revealed that ginseng has an inhibitory effect on Aβ pathology ( Lee et al, 2001 ; Kim et al, 2013 ; Choi et al, 2017 , 2020 ). Many human studies have also reported non-specific cognitive benefits of ginseng ( Geng et al, 2010 ; Lho et al, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Ginseng intake and Alzheimer disease-specific cognition in older adults according to apolipoprotein ε4 allele status

Lee

Choe

Suh

et al. 2023

Front. Aging Neurosci.

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BackgroundThe probable association among ginseng intake, Alzheimer’s disease (AD)-specific cognition, and apolipoprotein ε4 (APOE4) remains poorly investigated. Hence, we examined the association between ginseng intake and AD-specific cognition in older adults under the moderating effect of APOE4 status.MethodsThis study enrolled 160 adults aged 65–90 years without dementia. All participants underwent comprehensive dietary and clinical assessments including ginseng intake, AD-related cognition (i.e., delayed episodic memory, as the earliest cognitive change in AD), and non-memory cognition for comparative purposes.ResultsGinseng intake was associated with higher delayed episodic memory, but not non-memory cognition, compared to no ginseng intake. The interaction between ginseng intake and APOE4 status had a significant effect on delayed episodic memory. Subgroup analyses showed that ginseng intake was associated with higher delayed episodic memory in the APOE4-negative but not the APOE4-positive subgroup. The benefits of ginseng intake on delayed episodic memory were prominent in the high duration (≥5 years) and midlife onset (<65 years) groups.ConclusionOur study of older adults with no dementia suggests that ginseng intake (with high duration and midlife onset) had a beneficial effect on AD-specific cognitive decline, i.e., the delayed episodic memory. In addition, APOE4 status moderates the association between ginseng intake status and AD-specific cognitive decline.

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Korean Red Ginseng Inhibits Amyloid-β-Induced Apoptosis and Nucling Expression in Human Neuronal Cells

Cited by 10 publications

References 38 publications

Neuroprotective effects of donepezil against Aβ25-35-induced neurotoxicity

Neuroprotective effects of donepezil against Aβ25-35-induced neurotoxicity

Regulation of mitochondrial dysfunction induced cell apoptosis is a potential therapeutic strategy for herbal medicine to treat neurodegenerative diseases

Ginseng intake and Alzheimer disease-specific cognition in older adults according to apolipoprotein ε4 allele status

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