2,3,5,4′-Tetrahydroxystilbene-2-O-β-d-glucoside Restores BDNF-TrkB and FGF2-Akt Signaling Axis to Attenuate Stress-induced Depression

Li, Xixi; Yu, Yun; Lang, Xiu-Yuan; Jiang, Cheng-Yong; Lan, Rongfeng; Qin, Xiao-Yan

doi:10.1016/j.neuroscience.2020.01.025

Cited by 16 publications

(11 citation statements)

References 23 publications

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“…THSG promotes the expression of the longevity gene Klotho and attenuates MPP+-induced neurotoxicity in SH-SY5Y and PC12 cells 1 , 7 , 18 . THSG also prevents chronic restraint stress-induced depression-like behaviors in a mouse model by reducing oxidative stress and inflammatory responses 1 , 5 . Pharmacokinetic analysis showed that THSG was rapidly absorbed by the gastrointestinal tract and conjugated with α- D -glucuronic acid to form intermediate substance and further metabolized.…”

Section: Discussionmentioning

confidence: 99%

“…Accordingly, THSG is effective to ameliorate the neural death in PD mice, possibly through restoring the expression of brainderived neurotrophic factor (BDNF) and its associated TrkB/Akt signaling pathway [7]. We and colleagues reported the role of BDNF in THSG mediated anti-depressant-like effects in mild stress induced depressive mice [5,8]. Recovery the expression of BDNF may be a potential strategy for therapy of depression, schizophrenia, AD and PD, etc.…”

Section: Introductionmentioning

confidence: 99%

“… 1 - 4 . In particular, 2,3,5,4'-tetrahydoxystilbene-2-O-β-D-glucoside (THSG) is the characteristic chemical and has been well established for its functions in promoting longevity, anti-depression, attenuating inflammation, anti-aging and aging related diseases 4 , 5 . Thus, the neuroprotective effects of THSG have been recognized increasingly.…”

Section: Introductionmentioning

confidence: 99%

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2,3,5,4'-tetrahydoxystilbene-2-O-β-D-glucoside eliminates staurosporine-induced cytotoxicity by restoring BDNF-TrkB/Akt signaling axis

et al. 2020

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2,3,5,4'-Tetrahydroxystilbene-2-O-β-d-glucoside (THSG) is the major active ingredient in Plygonum multiflorum that displays a great deal of health-benefits including anti-oxidation, anti-hyperlipidemia, anti-cancer, anti-inflammation and neuroprotection. However, it is unclear whether THSG exerts neuroprotective functions by regulating neurotrophic factors and their associated signaling pathways. In this study, hippocampal neurons were challenged with staurosporine (STS) to establish a neural damage model. We found that STS-induced cytotoxicity introduced significant morphological collapse and initiating cell apoptosis, along with the down regulation of BDNF and TrkB/Akt signaling axis. In contrast, neurons pretreated with THSG showed resistance to STS-induced toxicity and maintained cell survival. THSG rescued STS induced dysfunctions of BDNF and its associated TrkB/Akt signaling, and restored the expression of Bcl-2 and Caspase-3. However, inhibition of TrkB activity by K252a or Akt signaling by LY294002 abolished the neuroprotective effects of THSG. Therefore, BDNF and TrkB/Akt signaling axis is a promise target for THSG mediated neuroprotective functions.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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2,3,5,4'-tetrahydoxystilbene-2-O-β-D-glucoside eliminates staurosporine-induced cytotoxicity by restoring BDNF-TrkB/Akt signaling axis

et al. 2020

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“…Activation of AKT ameliorates the effects of chronic social defeat, which is causally related to major depression [ 163 ]. In a previous study, the compound, Dl-3-n-butylphthalide, attenuated mouse behavioral deficits via activation of the AKT signaling pathway in the hippocampus of chronic social defeat stress-induced depressive mice [ 164 ], and a similar phenomenon was observed in the prefrontal cortex of chronic-restraint stress induced depression-like mice [ 165 ]. Also, SIRT6 overexpression in hippocampal neurons induced depressive behaviors via inhibition of the AKT signaling pathway in depressed rodents [ 166 ].…”

Section: The Roles Of Akt In Mitochondria-related Diseasesmentioning

confidence: 96%

Mammalian AKT, the Emerging Roles on Mitochondrial Function in Diseases

Xie¹,

Shu²,

Yu³

et al. 2022

Aging and disease

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Mitochondrial dysfunction may play a crucial role in various diseases due to its roles in the regulation of energy production and cellular metabolism. Serine/threonine kinase (AKT) is a highly recognized antioxidant, immunomodulatory, anti-proliferation, and endocrine modulatory molecule. Interestingly, increasing studies have revealed that AKT can modulate mitochondria-mediated apoptosis, redox states, dynamic balance, autophagy, and metabolism. AKT thus plays multifaceted roles in mitochondrial function and is involved in the modulation of mitochondria-related diseases. This paper reviews the protective effects of AKT and its potential mechanisms of action in relation to mitochondrial function in various diseases.

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“…It is also present in the prefrontal cortex [7,9], cerebellum [4], amygdala [58][59][60] and hypothalamus [4,58]. These areas are involved with the pathophysiology of depression [61][62][63][64].…”

Section: Brain-derived Neurotrophic Factormentioning

confidence: 99%

BDNF, A Focus to Major Depression

Nazareth¹

2021

OJP

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Major depressive disorder is characterized, among other symptoms, by depressed mood and anhedonia associated with a high rate of suicidal ideation. In recent years, research has shown reduced expression of the brain-derived neurotrophic factor (BDNF) in limbic areas of individuals with depression. This reduction of BDNF is reversed by antidepressants in animal models of stress. Stress is one of the main triggers of mood disorders such as depression. Also, administration of BDNF increases the number of serotonergic fibers and serotonergic innervation, indicating an increase of serotonin in the synaptic cleft by this neurotrophin. Thus, BDNF appears to be one of the targets of antidepressant drugs for the increase of monoamines and remission of symptoms of major depression. The purpose of this review was to show the evidence that indicates BDNF as a molecular substrate for vulnerability to depression and the response of this substrate to the antidepressants.

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2,3,5,4′-Tetrahydroxystilbene-2-O-β-d-glucoside Restores BDNF-TrkB and FGF2-Akt Signaling Axis to Attenuate Stress-induced Depression

Cited by 16 publications

References 23 publications

2,3,5,4'-tetrahydoxystilbene-2-O-β-D-glucoside eliminates staurosporine-induced cytotoxicity by restoring BDNF-TrkB/Akt signaling axis

2,3,5,4'-tetrahydoxystilbene-2-O-β-D-glucoside eliminates staurosporine-induced cytotoxicity by restoring BDNF-TrkB/Akt signaling axis

Mammalian AKT, the Emerging Roles on Mitochondrial Function in Diseases

BDNF, A Focus to Major Depression

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