Protective effect of ginsenoside Rb1 against chronic restraint stress (CRS)-induced memory impairments in rats

Jiang, Ning; Wang, Kezhu; Zhang, Yiwen; Huang, Hong; Lv, Jingwei; Wang, Qiong; Wang, Haixia; Xia, Tianji; Liu, Xinmin

doi:10.1016/j.bbr.2021.113146

Cited by 13 publications

(9 citation statements)

References 42 publications

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“…Synaptic plasticity, the ability of neurons to change the structure or function of their synapses, is the basis for learning and memory . Based on several research studies, upregulating synaptic plasticity can ameliorate cognitive function. − BDNF is crucial in regulating synaptic plasticity. − PSD-95 is a key component of postsynaptic density and SYP is a membrane protein of presynaptic vesicles, both of which are inextricably linked to learning and memory. − Thus, the expression of BDNF, SYP, and PSD-95 was detected to indirectly analyze synaptic plasticity. For directly analyzing synaptic plasticity, spine density and dendritic length were measured, as well as Sholl analysis.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of 20(S)-Protopanaxadiol on D-Gal-Induced Cognitively Impaired Mice Based on Its Target Protein Brain-type Creatine Kinase

Zhang

Chen

et al. 2023

J. Agric. Food Chem.

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Ginseng is an important medicinal herb consumed as dietary supplements. Ginsenosides and their metabolites have been reported to enhance cognitive performance, but their underlying mechanisms remain unclear. Brain-type creatine kinase (CK-BB) was previously screened out as one of the potential targets in brain tissues. In vitro, the strongest direct interaction between 20(S)-protopanaxadiol (PPD), a ginsenoside metabolite, and CK-BB was detected using biolayer interferometry (BLI). Drug affinity responsive target stability, cellular thermal shift assay, BLI, and isothermal titration calorimetry were subsequently used, and the binding of PPD to CK-BB was verified. The binding sites of the CK-BB/PPD complex were clarified by molecular docking and site-directed mutagenesis. Enzyme activity assay showed that the binding of PPD to CK-BB in vitro enhanced its activity. In vivo, PPD increased CK-BB activity in D-gal-induced mice. PPD also improved the D-gal-induced cognitive deficits and ameliorated alterations in oxidative stress and hippocampal synaptic plasticity. Therefore, the integration of PPD with its target protein CK-BB may promote CK-BB activity, thereby ameliorating hippocampal synaptic plasticity and cognitive deficits in D-gal-treated mice.

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Section: Discussionmentioning

confidence: 99%

Protective Effect of 20(S)-Protopanaxadiol on D-Gal-Induced Cognitively Impaired Mice Based on Its Target Protein Brain-type Creatine Kinase

Zhang

Chen

et al. 2023

J. Agric. Food Chem.

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“…Studies demonstrated that in an MPTP mouse model, treatment with Rb1 promoted LTP and glutamatergic and GABAergic transmission in the hippocampus of mice; the underlying mechanism was that Rb1 sequentially improved the expression of PSD95 and α-synuclein in hippocampal CA3 [ 66 , 145 ]. Rb1 also increased the density of a synaptic marker protein including synaptophysin PSD95 in a different pathological model such as chronic restraint stress as well as health animals [ 142 , 146 ]. Moreover, Rb1 administration promotes LTP and increased cell survival in the dentate gyrus and hippocampal CA3, suggesting that Rb1 enhanced not only synaptic plasticity but also neurogenesis [ 147 , 148 ].…”

Section: Pharmacological Properties Of Ginsenosides Of CImentioning

confidence: 99%

“…In ischemic stroke mice, PF11 preadministration improved CI and hippocampal atrophy; promoted neuronal generation and survival; and increased the expression of CREB, p-CREB, m-BDNF, and TrkB in the dentate gyrus and striatum, while these effects were eliminated by a specific inhibitor of TrkB in OGD/R-induced neural stem cells [ 194 ]. In the chronic restraint stress (CRS)-induced CI model, ginsenoside Rb1 could improve synaptic plasticity, inhibit apoptosis, and activate the BDNF/TrkB signaling pathway [ 146 ]. What is more, ginsenoside Rg1 repaired hippocampal LTP and memory, reduced Aβ 1–42 deposition and tau hyperphosphorylation, and upregulated the expression of BDNF and p-TrkB in both AD and aging mice [ 73 , 136 ].…”

Section: Signaling Pathways Involved In the Treatment Of CI By Ginsen...mentioning

confidence: 99%

Ginsenoside and Its Therapeutic Potential for Cognitive Impairment

et al. 2022

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Cognitive impairment (CI) is one of the major clinical features of many neurodegenerative diseases. It can be aging-related or even appear in non-central nerve system (CNS) diseases. CI has a wide spectrum that ranges from the cognitive complaint with normal screening tests to mild CI and, at its end, dementia. Ginsenosides, agents extracted from a key Chinese herbal medicine (ginseng), show great promise as a new therapeutic option for treating CI. This review covered both clinical trials and preclinical studies to summarize the possible mechanisms of how ginsenosides affect CI in different diseases. It shows that ginsenosides can modulate signaling pathways associated with oxidative stress, apoptosis, inflammation, synaptic plasticity, and neurogenesis. The involved signaling pathways mainly include the PI3K/Akt, CREB/BDNF, Keap1/Nrf2 signaling, and NF-κB/NLRP3 inflammasome pathways. We hope to provide a theoretical basis for the treatment of CI for related diseases by ginsenosides.

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“…Ginsenoside Rb1 exerted promising antidepressant-like effects in mice with chronic social defeat stress (CSDS)-induced depression by enhancing the BDNF/Trkb signaling cascade, which increased the hippocampal neurogenesis ( Jiang et al, 2021a ). Similarly, ginsenoside Rb1 treatment ameliorated chronic restraint stress (CRS)-induced memory impairments in rats by improving synaptic plasticity and restoring the BDNF/TrkB signalling pathway ( Jiang et al, 2021b ). Guo et al (2021) found that ginsenoside Rb1 not only increased the protein expression of BDNF, but also activated the pro-survival Akt pathway in CRS mice.…”

Section: Ginsenoside Rb1 In Depressionmentioning

confidence: 99%

Neuroprotective Mechanisms of Ginsenoside Rb1 in Central Nervous System Diseases

et al. 2022

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Panax ginseng and Panax notoginseng, two well-known herbs with enormous medical value in Asian countries, have a long usage history in China for the therapy of some diseases, such as stroke. Ginsenoside Rb1 is one of most important active ingredients in Panax ginseng and Panax notoginseng. In the last two decades, more attention has focused on ginsenoside Rb1 as an antioxidative, anti-apoptotic and anti-inflammatory agent that can protect the nervous system. In the review, we summarize the neuroprotective roles of ginsenoside Rb1 and its potential mechanisms in central nervous system diseases (CNSDs), including neurodegenerative diseases, cerebral ischemia injury, depression and spinal cord injury. In conclusion, ginsenoside Rb1 has a potential neuroprotection due to its inhibition of oxidative stress, apoptosis, neuroinflammation and autophagy in CNSDs and may be a promising candidate agent for clinical therapy of CNSDs in the future.

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Protective effect of ginsenoside Rb1 against chronic restraint stress (CRS)-induced memory impairments in rats

Cited by 13 publications

References 42 publications

Protective Effect of 20(S)-Protopanaxadiol on D-Gal-Induced Cognitively Impaired Mice Based on Its Target Protein Brain-type Creatine Kinase

Protective Effect of 20(S)-Protopanaxadiol on D-Gal-Induced Cognitively Impaired Mice Based on Its Target Protein Brain-type Creatine Kinase

Ginsenoside and Its Therapeutic Potential for Cognitive Impairment

Neuroprotective Mechanisms of Ginsenoside Rb1 in Central Nervous System Diseases

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