Ginsenoside Rb1 attenuates activated microglia-induced neuronal damage

Ke, Liyuan; Guo, Wei; Xu, Jun; Zhang, Guodong; Wang, Wei; Huang, Wenhua

doi:10.4103/1673-5374.128217

Cited by 26 publications

(15 citation statements)

References 43 publications

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“…These cytotoxic factors are the major cause of neuronal damage and neuronal apoptosis through regulation of the Bcl-2 family [54,55,56]. The Bcl-2 family consists of pro-apoptotic (Bax and cleaved caspase-3) and pro-survival (Bcl-2) proteins, which are responsible for the physical and functional interactions that regulate apoptosis [57].…”

Section: Discussionmentioning

confidence: 99%

Equol, a Dietary Daidzein Gut Metabolite Attenuates Microglial Activation and Potentiates Neuroprotection In Vitro

et al. 2017

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Estrogen deficiency has been well characterized in inflammatory disorders including neuroinflammation. Daidzein, a dietary alternative phytoestrogen found in soy (Glycine max) as primary isoflavones, possess anti-inflammatory activity, but the effect of its active metabolite Equol (7-hydroxy-3-(4′-hydroxyphenyl)-chroman) has not been well established. In this study, we investigated the anti-neuroinflammatory and neuroprotective effect of Equol in vitro. To evaluate the potential effects of Equol, three major types of central nervous system (CNS) cells, including microglia (BV-2), astrocytes (C6), and neurons (N2a), were used. Effects of Equol on the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX-2), Mitogen activated protein kinase (MAPK) signaling proteins, and apoptosis-related proteins were measured by western blot analysis. Equol inhibited the lipopolysaccharide (LPS)-induced TLR4 activation, MAPK activation, NF-kB-mediated transcription of inflammatory mediators, production of nitric oxide (NO), release of prostaglandin E2 (PGE-2), secretion of tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6), in Lipopolysaccharide (LPS)-activated murine microglia cells. Additionally, Equol protects neurons from neuroinflammatory injury mediated by LPS-activated microglia through downregulation of neuronal apoptosis, increased neurite outgrowth in N2a cell and neurotrophins like nerve growth factor (NGF) production through astrocytes further supporting its neuroprotective potential. These findings provide novel insight into the anti-neuroinflammatory effects of Equol on microglial cells, which may have clinical significance in cases of neurodegeneration.

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Section: Discussionmentioning

confidence: 99%

Equol, a Dietary Daidzein Gut Metabolite Attenuates Microglial Activation and Potentiates Neuroprotection In Vitro

et al. 2017

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“…For instance, ginsenosides Rg1, Rg3, Rh1, Rh3, Rb1, Rk1, and Rf from Panax ginseng C.A. Meyer have been demonstrated to exhibit dual actions against neuroinflammation and hyperactivation of the HPA axis [ 106 , 108 , 206 , 207 , 208 , 209 , 210 , 211 , 212 , 213 , 214 , 215 ], while 3,6’-disinapoyl sucrose and the oligosaccharide esters-enriched fraction, YZ50, from Polygala tenuifolia Willd have been shown to possess bioactivity that de-hyperactivates the HPA axis [ 216 , 217 , 218 ]. Additionally, poricoic acid A, isolated from Poria cocos (Schw.)…”

Section: Chm Effects On the Neuroendocrine-immune Networkmentioning

confidence: 99%

Chinese Herbal Medicine for the Treatment of Depression: Effects on the Neuroendocrine-Immune Network

Huang

Zhang

2021

Pharmaceuticals

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The neuroimmune and neuroendocrine systems are two critical biological systems in the pathogenesis of depression. Clinical and preclinical studies have demonstrated that the activation of the neuroinflammatory response of the immune system and hyperactivity of the hypothalamus–pituitary–adrenal (HPA) axis of the neuroendocrine system commonly coexist in patients with depression and that these two systems bidirectionally regulate one another through neural, immunological, and humoral intersystem interactions. The neuroendocrine-immune network poses difficulties associated with the development of antidepressant agents directed toward these biological systems for the effective treatment of depression. On the other hand, multidrug and multitarget Chinese Herbal Medicine (CHM) has great potential to assist in the development of novel medications for the systematic pharmacotherapy of depression. In this narrative essay, we conclusively analyze the mechanisms of action of CHM antidepressant constituents and formulas, specifically through the modulation of the neuroendocrine-immune network, by reviewing recent preclinical studies conducted using depressive animal models. Some CHM herbal constituents and formulas are highlighted as examples, and their mechanisms of action at both the molecular and systems levels are discussed. Furthermore, we discuss the crosstalk of these two biological systems and the systems pharmacology approach for understanding the system-wide mechanism of action of CHM on the neuroendocrine-immune network in depression treatment. The holistic, multidrug, and multitarget nature of CHM represents an excellent example of systems medicine in the effective treatment of depression.

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“…The reduction of neurological deficits, brain oedema and BBB permeability are argued to underlie BBB protection. Further to this Ke et al ( 2014 ) demonstrated that ginsenoside Rb1 attenuates damage to rat cerebral cortical neurons against hypoxia-activated microglia. This neuroprotective mechanism may be mediated by the downregulation of nitric oxide, superoxide, and TNF-α expression (Ke et al, 2014 ).…”

Section: Plant Based Extractsmentioning

confidence: 83%

The Immunomodulatory Effects of Plant Extracts and Plant Secondary Metabolites on Chronic Neuroinflammation and Cognitive Aging: A Mechanistic and Empirical Review

2017

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Advances in healthcare have considerably improved the life expectancy of the human population over the last century and this has brought about new challenges. As we live longer the capacity for cognitive aging increases. Consequently, it has been noted that decline in cognitive performance in the elderly in domains of reasoning, problem solving skills, attention, processing speed, working memory and episodic memory is a significant societal problem. Despite the enormity of this issue there are relatively few interventions for cognitive aging. This may be due to our current state of knowledge on biological factors that underpin cognitive aging. One of the biological contributors to cognitive aging is chronic neuroinflammation. This review will provide an overview of the peripheral and central mechanisms involved in chronic neuroinflammation and how neuroinflammation may be related to age-associated cognitive decline. Plant based extracts including herbal and nutritional supplements with anti-inflammatory properties will be examined in relation to their utility in treating age-related cognitive decline. Plant based extracts in particular offer interesting pharmacological properties that may be quickly utilized to prevent cognitive aging.

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Ginsenoside Rb1 attenuates activated microglia-induced neuronal damage

Cited by 26 publications

References 43 publications

Equol, a Dietary Daidzein Gut Metabolite Attenuates Microglial Activation and Potentiates Neuroprotection In Vitro

Equol, a Dietary Daidzein Gut Metabolite Attenuates Microglial Activation and Potentiates Neuroprotection In Vitro

Chinese Herbal Medicine for the Treatment of Depression: Effects on the Neuroendocrine-Immune Network

The Immunomodulatory Effects of Plant Extracts and Plant Secondary Metabolites on Chronic Neuroinflammation and Cognitive Aging: A Mechanistic and Empirical Review

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