Ginsenoside Rd attenuates beta-amyloid-induced tau phosphorylation by altering the functional balance of glycogen synthase kinase 3beta and protein phosphatase 2A

Li, Ling; Liu, Zhongfan; Liu, Juanfang; Tai, Xuhui; Hu, Xinghua; Liu, Xuedong; Z, Wu; Zhang, Guangyun; Shi, Ming; Zhao, Gang

doi:10.1016/j.nbd.2013.01.002

Cited by 44 publications

(29 citation statements)

References 40 publications

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“…For example, Ginsenoside Rb1, Rg1, and Rg3 displayed protective effects against Aβ production and aggregation through mechanisms possibly including reduction of APP expression, inhibition on β-secretase activity as well as stimulation of α-secretase activity232425. In addition, Rg1and Rd prevented Aβ-induced neurotoxicity such as mitochondrial dysfunction, tau hyperphosphorylation as well as neuronal death262728. Furthermore, ginsenosides remarkably improved cognitive performance of AD patients and rodent models293031.…”

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confidence: 98%

Notoginsenoside R1 increases neuronal excitability and ameliorates synaptic and memory dysfunction following amyloid elevation

Yan

et al. 2014

Sci Rep

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Neurodegeneration and synaptic dysfunction observed in Alzheimer's disease (AD) have been associated with progressive decrease in neuronal activity. Here, we investigated the effects of Notoginsenoside R1 (NTR1), a major saponin isolated from Panax notoginseng, on neuronal excitability and assessed the beneficial effects of NTR1 on synaptic and memory deficits under the Aβ-enriched conditions in vivo and in vitro. We assessed the effects of NTR1 on neuronal excitability, membrane ion channel activity, and synaptic plasticity in acute hippocampal slices by combining electrophysiological extracellular and intracellular recording techniques. We found that NTR1 increased the membrane excitability of CA1 pyramidal neurons in hippocampal slices by lowering the spike threshold possibly through a mechanism involving in the inhibition of voltage-gated K+ currents. In addition, NTR1 reversed Aβ1-42 oligomers-induced impairments in long term potentiation (LTP). Reducing spontaneous firing activity with 10 nM tetrodotoxin (TTX) abolished the protective effect of NTR1 against Aβ-induced LTP impairment. Finally, oral administration of NTR1 improved the learning performance of the APP/PS1 mouse model of AD. Our work reveals a novel mechanism involving in modulation of cell strength, which contributes to the protective effects of NTR1 against Aβ neurotoxicity.

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confidence: 98%

Notoginsenoside R1 increases neuronal excitability and ameliorates synaptic and memory dysfunction following amyloid elevation

Yan

et al. 2014

Sci Rep

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“…An imbalance in the protein kinase and phosphatase system induces Tau protein phosphorylation, resulting in the formation of an abnormally phosphorylated Tau protein (19,20). Cis-trans prolyl isomerization, particularly following phosphorylation, has revealed that cis p-Tau is an early pathogenic conformation that leads to Tau pathology and memory loss in patients with AD (21).…”

Section: Discussionmentioning

confidence: 99%

Panax notoginsenoside Rb1 ameliorates Alzheimer’s disease by upregulating brain-derived neurotrophic factor and downregulating Tau protein expression

Wang

Feng

et al. 2013

Experimental and Therapeutic Medicine

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Alzheimer’s disease (AD) is a neurodegenerative disorder and the main cause of dementia. Panax notoginsenoside Rb1 (PNRb1), which is also known as (3β,12β)-20-[(6-O-β-D-glucopyranosyl-β-D-glucopyranosyl)oxy]-12-hydroxydammar-24-en-3-yl 2-O-β-D-glucopyranosyl-β-D-glucopyranoside and is the main active component of the plant Panax notoginseng, is effective in treating AD. However, the mechanisms of PNRb1 remain unknown. In the present study, rat brain tissue sections were pretreated with PNRb1 and then induced by okadaic acid to establish brain slice models of AD. The results of qPCR and immunoblot analyses demonstrated that PNRb1 suppressed the protein expression of phosphorylated Tau and upregulated the expression levels of brain-derived neurotrophic factor (BDNF). These results suggest that PNRb1 is able to upregulate the protein level of BDNF and downregulate Tau protein phosphorylation in AD.

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“…Although Rd is only present in trace quantities, it is one of the most potent ingredients in P. ginseng [36,43,49]. In 2000, Kim et al [3] isolated three human intestinal bacterial strains: Eubacterium sp., Streptococcus sp.…”

Section: Major Ginsenosides: Backgroundmentioning

confidence: 99%

“…The best-described biological activity of ginsenoside Rd is related to neurogenesis [47,62], neuroprotective [43] and anti-ischemic effects [19,49] (Table 1). In 2012, Zhao's group conducted a clinical study to elucidate the effect of ginsenoside Rd on acute ischemic stroke in 390 patients.…”

Section: Biological Activitiesmentioning

confidence: 99%

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Ginsenosides and their metabolites: a review of their pharmacological activities in the skin

et al. 2015

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Ginsenosides are representative pharmaceutical compounds found in various forms in Panax ginseng, a traditional medicinal plant. They are converted to their metabolites Rg2, Rg3, compound K, and others by human intestinal microflora following ingestion. Numerous studies have demonstrated beneficial effects of ginsenosides against aberrant molecular processes responsible for cancer, metabolic diseases and neurodegenerative diseases. Recently, antiaging effects of ginsenosides in human skin have been reported from clinical trial and in vitro model data. Ginsenosides have hence been proposed as promising natural cosmeceutical agents. In this review, we will critically review the known biological effects of several ginsenosides (Rb1, Rg3, Rd and compound K), such as anti-inflammatory and anticancer activities, which arise from the modulation of diverse molecular pathways. The application potential of ginsenosides as cosmeceutical ingredients will also be reviewed.

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Ginsenoside Rd attenuates beta-amyloid-induced tau phosphorylation by altering the functional balance of glycogen synthase kinase 3beta and protein phosphatase 2A

Cited by 44 publications

References 40 publications

Notoginsenoside R1 increases neuronal excitability and ameliorates synaptic and memory dysfunction following amyloid elevation

Notoginsenoside R1 increases neuronal excitability and ameliorates synaptic and memory dysfunction following amyloid elevation

Panax notoginsenoside Rb1 ameliorates Alzheimer’s disease by upregulating brain-derived neurotrophic factor and downregulating Tau protein expression

Ginsenosides and their metabolites: a review of their pharmacological activities in the skin

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