Preclinical systematic review of ginsenoside Rg1 for cognitive impairment in Alzheimer’s disease

Liang, Haiyong; Zhang, Peipei; Zhang, Xile; Huang, Yanran; Zheng, Guo-Qing

doi:10.18632/aging.202619

Cited by 29 publications

(23 citation statements)

References 91 publications

(60 reference statements)

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“…Ginsenoside Rg1 could improve the cognitive impairment of the AD tree shrews by reducing the deposition of Aβ1‐42 and phosphorylation of Tau. Ginsenoside is the main active ingredient of ginseng, and ginsenoside Rg1 (Rg1) is effective against AD in vivo or in vitro (Ardah et al, 2015; Liang et al, 2021; Nah et al, 2007). Our previous studies have shown that ginsenoside Rg1 improves cognitive function and reduces Aβ deposition and Tau phosphorylation in tree shrews with AD (Guo et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rg1 improves Alzheimer's disease by regulating oxidative stress, apoptosis, and neuroinflammation through Wnt/GSK‐3β/β‐catenin signaling pathway

et al. 2022

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Alzheimer's disease (AD) is a chronic neurodegenerative disorder that can cause cognitive impairment. Ginsenoside Rg1 (Rg1) has a significant neuroprotective effect on animals with memory impairment. However, the mechanism of how Rg1 mediates the Wnt signaling pathway and improves cognitive function by regulating oxidative stress, apoptosis, and neuroinflammation is still unclear. In this study, the spatial memory ability of tree shrews was tested by Morris water maze, the expression levels of amyloid protein (Aβ1-42), ionized calcium-binding adapter molecule 1 (iba-1), nitrotyrosine (NT), and 8-hydroxyguanine (8-OHG) were detected by immunohistochemistry. Subsequently, the activity of catalase (CAT) and the glutathione peroxidase (GSH-Px) was, respectively, measured by the ammonium molybdate method and the 5,5′-dithiobis (2-nitrobenzoic acid).Furthermore, the malondialdehyde (MDA) concentration was determined by the thiobarbituric acid test. Finally, the expression levels of Beta-secretase (BACE1), superoxide dismutase (SOD), BCL2-Associated X (Bax), B-cell lymphoma-2 (Bcl-2), caspase-anti-apoptotic factor Cleaved-caspase-3 (Caspase-3), microtubuleassociated proteins 2 (MAP2), Neuronal nuclear antigen (NeuN), as well as the phosphorylation of GSK-3β and βcatenin were detected by Western blot. This study implied that Rg1 reduced the phosphorylation of Tau protein, the deposition of Aβ1-42, and the expression of BACE1. It also showed that Rg1 increased the antioxidant activity of SOD, CAT, GPx, and instead reduced the oxidation products of NT, 8-OHG, and MDA, as wells as the inflammatory factor interleukin-1 and iba-1. It further showed that Rg1 increased the ratio of Bcl-2 to Bax and expression of neuronal markers MAP2 and NeuN, but instead reduced the expression of Caspase-3, GSK-3β, and β-catenin. In conclusion, by regulating the Wnt/GSK-3β/β-catenin signaling pathway, Rg1 of moderate and high dose could alleviate oxidative stress damage, improve neuroinflammation, protect neurons,

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Section: Discussionmentioning

confidence: 99%

Ginsenoside Rg1 improves Alzheimer's disease by regulating oxidative stress, apoptosis, and neuroinflammation through Wnt/GSK‐3β/β‐catenin signaling pathway

et al. 2022

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Section: Pharmacological Actionsmentioning

confidence: 99%

“…According to various cognitive‐behavioral tests, the meta‐analysis results showed that ginsenoside Rg1 significantly improved cognitive‐behavioral impairments in most animal models of AD ( p < 0.05) (Liang et al, 2021). The potential mechanisms includs antioxidant and anti‐inflammatory effects, amelioration of AD‐related pathology, synapse protection, and up‐regulation of nerve cells via multiple signaling pathways (Liang et al, 2021). Li et al (Li, Wu, Li, & Niu, 2016) found that ginsenoside Rg1 restored hippocampal long‐term potentiation and memory in the transgenic AD model, possibly by promoting the clearance of AD‐related proteins and by activating the brain‐derived neurotrophic factor (BDNF)‐tropomyosin‐related kinase B (TrkB) pathway.…”

Section: Pharmacological Actionsmentioning

confidence: 99%

Ginsenosides in central nervous system diseases: Pharmacological actions, mechanisms, and therapeutics

Xian

et al. 2022

Phytotherapy Research

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The nervous system is one of the most complex physiological systems, and central nervous system diseases (CNSDs) are serious diseases that affect human health. Ginseng (Panax L.), the root of Panax species, are famous Chinese herbs that have been used for various diseases in China, Japan, and Korea since ancient times, and remain a popular natural medicine used worldwide in modern times. Ginsenosides are the main active components of ginseng, and increasing evidence has demonstrated that ginsenosides can prevent CNSDs, including neurodegenerative diseases, memory and cognitive impairment, cerebral ischemia injury, depression, brain glioma, multiple sclerosis, which has been confirmed in numerous studies. Therefore, this review summarizes the potential pathways by which ginsenosides affect the pathogenesis of CNSDs mainly including antioxidant effects, anti-inflammatory effects, anti-apoptotic effects, and nerve protection, which provides novel ideas for the treatment of CNSDs.

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“…Ginsenosides, the main active ingredients of ginseng, play an important role in the central nervous system (CNS) disorders and widely act on cell membrane receptors [34]. Several studies have demonstrated that ginsenoside Rg1 could improve cognitive function in chemotherapyinduced cognitive impairment, repeated alcohol exposureinduced cognitive deficits, and Alzheimer's disease [12,35,36]. Moreover, ginsenoside Rg1 has ameliorative effects on various brain injuries, such as focal cerebral ischemia injury, diabetic complicated cerebral infarction, and ischemicreperfusion brain injury [37][38][39].…”

Section: Neural Plasticitymentioning

confidence: 99%

“…[9][10][11]. Especially, Rg1 has been extensively investigated in the treatment of dementia, such as improving cognitive dysfunction in mice with Alzheimer's disease [12]. Intriguingly, Rg1 was also reported to prevent cognitive impairment and neuronal damage in VD rats [13], but leaving the mechanisms largely open.…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rg1 Prevents Cognitive Impairment and Hippocampal Neuronal Apoptosis in Experimental Vascular Dementia Mice by Promoting GPR30 Expression

Shen

Wang

et al. 2021

Neural Plasticity

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This study is aimed at investigating the potential roles of G protein-coupled estrogen receptor 1 (GPER, also known as GPR30) in the preventive effect of ginsenoside Rg1 against cognitive impairment and hippocampal cell apoptosis in experimental vascular dementia (VD) in mice. The effects of bilateral common carotid artery stenosis (BCAS) on GPR30 expression at mRNA level were evaluated. Thereafter, the BCAS mouse model was utilized to evaluate the protection of Rg1 (0.1, 1, 10 mg/kg, 14 days, ip). Spatial memory was evaluated by water Morris Maze 7 days post BCAS. After behavioral tests, neuronal apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay, and potential mechanisms were determined using western blotting and quantitative real-time PCR. Our results showed that GPR30 expression in the hippocampal region at mRNA level was promoted 30 min, 3 h, 6 h, and 24 h following BCAS. Ginsenoside Rg1 (1 or 10 mg/kg, 14 days, ip) promoted GPR30 expression in the hippocampus of model mice (after behavioral tests) but did not alter GPR30 expression in the hippocampus of control mice. Moreover, treatment of ginsenoside Rg1 (10 mg/kg) or G1 (5 μg/kg), a GPR30 agonist, prevented BCAS-induced memory impairment and hippocampal neuronal loss and apoptosis and promoted the ratio of Bcl-2 to Bax expression in the hippocampus (after behavioral tests). On the contrary, G15 (185 μg/kg), an antagonist of GPR30, aggravated BCAS-induced hippocampal neuronal loss and apoptosis. Finally, drug-target molecular docking pointed that Rg1 had a lower binding energy with GPR30 compared with Bax and Bcl-2. Together, our data implicate that ginsenoside Rg1 prevents cognitive impairment and hippocampal neuronal apoptosis in VD mice, likely through promoting GPR30 expression. These results would provide important implications for the application of Rg1 in the treatment of VD.

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Preclinical systematic review of ginsenoside Rg1 for cognitive impairment in Alzheimer’s disease

Cited by 29 publications

References 91 publications

Ginsenoside Rg1 improves Alzheimer's disease by regulating oxidative stress, apoptosis, and neuroinflammation through Wnt/GSK‐3β/β‐catenin signaling pathway

Ginsenoside Rg1 improves Alzheimer's disease by regulating oxidative stress, apoptosis, and neuroinflammation through Wnt/GSK‐3β/β‐catenin signaling pathway

Ginsenosides in central nervous system diseases: Pharmacological actions, mechanisms, and therapeutics

Ginsenoside Rg1 Prevents Cognitive Impairment and Hippocampal Neuronal Apoptosis in Experimental Vascular Dementia Mice by Promoting GPR30 Expression

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