Protective effects of SGB121, ginsenoside F1-enriched ginseng extract, on scopolamine-induced cytotoxicity and memory impairments

Bastola, Tonking; Pariyar, Ramesh; Jeon, Byeong Min; Baek, Jong-In; Chang, Bo Yoon; Kim, Sun-Chang; Kim, Sung Yeon; Seo, Jooyeok

doi:10.1016/j.jff.2020.104165

Cited by 6 publications

(4 citation statements)

References 71 publications

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“…These findings are concurrent with previous studies reporting mitigation of scopolamine-induced memory impairment through BDNF/ERK-Akt/CREB activation. 35,50,51 As expected, donepezil also reduced the TNF-α expression and increased the levels of CREB and BDNF in scopolamine-induced mice. With this set of data and the existing literature, it is quite intriguing to draw a conclusive link between the mode of action of wheatgrass and activation of the ERK/Akt-CREB-BDNF signaling pathway.…”

Section: Discussionsupporting

confidence: 67%

Wheatgrass extract imparts neuroprotective actions against scopolamine-induced amnesia in mice

et al. 2022

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Section: Discussionsupporting

confidence: 67%

Wheatgrass extract imparts neuroprotective actions against scopolamine-induced amnesia in mice

et al. 2022

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“…Meanwhile, the control, positive, and memory impairment model groups were administered equal volumes of 0.9% normal saline. At 6 weeks, all of the groups were injected with scopolamine solution (1 mg/kg bw) to induce the amnesia mouse model except for the control group, , and the positive group was administered piracetam solution (400 mg/kg bw). The behavioral test was carried out 30 min later by the WMT-100 Morris water maze video analysis system (Chengdu Taimeng Software Co., Ltd., Chengdu, China).…”

Section: Methodsmentioning

confidence: 99%

Walnut-Derived Peptide Activates PINK1 via the NRF2/KEAP1/HO-1 Pathway, Promotes Mitophagy, and Alleviates Learning and Memory Impairments in a Mice Model

Zhao

et al. 2021

J. Agric. Food Chem.

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Mitophagy has a pivotal protective function in the pathogenesis of neurological disorders. However, the mechanism of its modulation remains elusive, especially in PINK1-mediated mitophagy. Here, we investigated the neuroprotective effects of a walnut-derived peptide, YVLLPSPK, against scopolamine-induced cognitive deficits in mice and explored the underlying PINK1mediated mitophagy mechanisms in H 2 O 2 -treated HT-22 cells. Using the Morris water maze, we showed that YVLLPSPK relieved the cognitive deficiency by alleviating oxidative stress. Mitochondrial morphology was observed in mice hippocampal tissues using transmission electron microscopy (TEM). Both Western blot and immunofluorescence analysis illustrated YVLLPSPK promoted the expression of mitophagy-related proteins and activated the NRF2/KEAP1/HO-1 pathway. Subsequently, an NRF2 inhibitor (ML385) was used to verify the contribution of the YVLLPSPK-regulated NRF2/KEAP1/HO-1 pathway in PINK1-mediated mitophagy in H 2 O 2 -treated HT-22 cells. These data suggested that YVLLPSPK improved learning and memory in scopolamineinduced cognitive-impaired mice through a mechanism associated with PINK1-mediated mitophagy via the NRF2/KEAP1/HO-1 pathway.

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“…Importantly, our previous results indicated that F1 is able to attenuate glials-derived inflammation induced by oxidative stress [44]. Additionally, F1-enrich mixture effectively protect brain from scopolamine-induced cytotoxicity and memory impairments [45]. Thus, ginsenoside F1 is a promising candidate for targeting AD and other brain pathologies.…”

Section: Discussionmentioning

confidence: 98%

Ginsenoside F1 Protects the Brain against Amyloid Beta-Induced Toxicity by Regulating IDE and NEP

Yun

Park

Hou

et al. 2022

Life

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Ginsenoside F1, the metabolite of Rg1, is one of the most important constituents of Panax ginseng. Although the effects of ginsenosides on amyloid beta (Aβ) aggregation in the brain are known, the role of ginsenoside F1 remains unclear. Here, we investigated the protective effect of ginsenoside F1 against Aβ aggregation in vivo and in vitro. Treatment with 2.5 μM ginsenoside F1 reduced Aβ-induced cytotoxicity by decreasing Aβ aggregation in mouse neuroblastoma neuro-2a (N2a) and human neuroblastoma SH-SY5Y neuronal cell lines. Western blotting, real-time PCR, and siRNA analysis revealed an increased level of insulin-degrading enzyme (IDE) and neprilysin (NEP). Furthermore, liquid chromatography with tandem mass spectrometry (LC-MS/MS) analysis confirmed that ginsenoside F1 could pass the blood–brain barrier within 2 h after administration. Immunostaining results indicate that ginsenoside F1 reduces Aβ plaques in the hippocampus of APPswe/PSEN1dE9 (APP/PS1) double-transgenic Alzheimer’s disease (AD) mice. Consistently, increased levels of IDE and NEP protein and mRNA were observed after the 8-week administration of 10 mg/kg/d ginsenoside F1. These data indicate that ginsenoside F1 is a promising therapeutic candidate for AD.

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Protective effects of SGB121, ginsenoside F1-enriched ginseng extract, on scopolamine-induced cytotoxicity and memory impairments

Cited by 6 publications

References 71 publications

Wheatgrass extract imparts neuroprotective actions against scopolamine-induced amnesia in mice

Wheatgrass extract imparts neuroprotective actions against scopolamine-induced amnesia in mice

Walnut-Derived Peptide Activates PINK1 via the NRF2/KEAP1/HO-1 Pathway, Promotes Mitophagy, and Alleviates Learning and Memory Impairments in a Mice Model

Ginsenoside F1 Protects the Brain against Amyloid Beta-Induced Toxicity by Regulating IDE and NEP

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