Alpinia oxyphylla Miq. and Its Active Compound P-Coumaric Acid Promote Brain-Derived Neurotrophic Factor Signaling for Inducing Hippocampal Neurogenesis and Improving Post-cerebral Ischemic Spatial Cognitive Functions

He, Yacong; Chen, Shuang; Tsoi, Bun; Qi, Shihua; Gu, Bing; Wang, Zhenxing; Peng, Cheng; Shen, Jiangang

doi:10.3389/fcell.2020.577790

Cited by 30 publications

(32 citation statements)

References 55 publications

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“…A large amount of in vitro studies revealed that propofol may improve BBB function (Chen et al 2019), protect neuron apoptosis (Xu et al 2017) and autophagy (Li et al 2020), and maintain microglia function ). In addition, animal studies demonstrated that propofol may improve brain function in rats with ischemia-reperfusion injury (Chen et al 2021) and may ameliorate neuroin ammatory injury in rats (Ma et al 2020, Jiang et al 2021.…”

Section: Discussionmentioning

confidence: 99%

“…However, accumulating evidence suggested that mature BDNF has high a nity to TrkB, while its precursor proBDNF mainly activates p75 NTR (Chao et al .1995). Numerous in vitro and animal studies revealed that multiple pathophysiological stimuli such as oxidative stress, in ammation, and ischemia/reperfusion injury may induce damages in the CNS via affecting BDNF/TrkB signaling (Colucci-D'Amato et al 2020), and recently, BDNF/TrkB signaling has been identi ed to serve as a potential therapeutic target for depression (Zhang et al 2016), post-cerebral ischemic spatial cognitive dysfunction (He et al 2021), vascular dementia (Wang et al 2020) and postoperative cognitive dysfunction (Qiu et al 2020).…”

Section: Introductionmentioning

confidence: 99%

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The Effect of Propofol on Hypoxia- and TNF-α-Mediated Brain-Derived Neurotrophic Factor/Tyrosine Kinase Receptor B Pathway Dysregulation in Primary Rat Hippocampal Neurons

Tao

Ding

et al. 2021

Preprint

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Background: Brain-derived neurotrophic factor/tyrosine kinase receptor B (BDNF/TrkB) pathway dysregulation may be induced by hypoxia and inflammation, and play pivotal roles during the development of neurological disorders. Propofol is an anesthetic agent with neuro-protective properties. We aimed to verify whether propofol affected BDNF/TrkB pathway in neurons and astrocytes exposed to hypoxia and inflammation.Methods: Primary rat hippocampal neurons and astrocytes were cultured and exposed to propofol followed by hypoxia or TNF-α treatment. The production of BDNF and the expression/truncation/phosphorylation of TrkB were measured. The underlying mechanisms such as ERK, CREB, p35 and Cdk5 were investigated.Results: In hippocampal neurons and astrocytes, hypoxia and TNF-α reduced the production of BDNF. Pretreatment of hippocampal neurons with 25μM propofol reversed the inhibitory effect of hypoxia or TNF-α on BDNF production. However, even 100μM propofol had no such effect in astrocytes. Further, we found that in hippocampal neurons hypoxia and TNF-α increased the phosphorylation of ERK (p-ERK) and CREB at Ser142 (p-CREB Ser142), while reduced the phosphorylation of CREB at Ser133 (p-CREB Ser133), which were all reversed by 25μM propofol and 10μM ERK inhibitor. In addition, we reported that hypoxia- and TNF-α-mediated reduction of BDNF was mitigated by 10μM ERK inhibitor, and the beneficial effect of propofol was abolished by 10μM ERK activator. We also found neither hypoxia nor TNF-α affected TrkB expression, truncation or phosphorylation in hippocampal neurons and astrocytes. However 50μM propofol induced TrkB phosphorylation without affecting its expression and truncation only in hippocampal neurons. Furthermore, we detected that in hippocampal neurons, 50μM propofol induced p35 expression and Cdk5 activation, and blockade of p35 or Cdk5 mitigated propofol-induced TrkB phosphorylation.Conclusions: Propofol, via ERK/CREB and p35/Cdk5, may modulate BDNF/TrkB pathway in hippocampal neurons that were exposed to hypoxia or TNF-α.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Effect of Propofol on Hypoxia- and TNF-α-Mediated Brain-Derived Neurotrophic Factor/Tyrosine Kinase Receptor B Pathway Dysregulation in Primary Rat Hippocampal Neurons

Tao

Ding

et al. 2021

Preprint

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“…The neuroprotective activity of p-CA was also confirmed in pheochromocytoma PC12 cells where it suppressed formation of ROS [102], attenuated beta amyloid-induced apoptosis [103,104], and inhibited expression of inflammatory target proteins via inactivation of NF-κB and MAPKs signaling pathways [105]. Recent in vivo and in vitro experiments showed that p-CA promoted neural stem cell proliferation via activation of brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB)/AKT signaling pathway, improved spatial learning and memory functions, and reduced anxiety in post-ischemic stroke rats [106]. Thus, the beneficial effects of p-coumaric acid are mainly related to its ability of inducing BDNF-TrkB signaling regulation, mediate expression of apoptotic factors such as TLR4, IL-6, TGFβ1 and inhibiting amyloid fibrillogenesis.…”

Section: P-coumaric Acidmentioning

confidence: 99%

The Use of Bioactive Compounds in Hyperglycemia- and Amyloid Fibrils-Induced Toxicity in Type 2 Diabetes and Alzheimer’s Disease

2022

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It has become increasingly apparent that defective insulin signaling may increase the risk for developing Alzheimer’s disease (AD), influence neurodegeneration through promotion of amyloid formation or by increasing inflammatory responses to intraneuronal β-amyloid. Recent work has demonstrated that hyperglycemia is linked to cognitive decline, with elevated levels of glucose causing oxidative stress in vulnerable tissues such as the brain. The ability of β-amyloid peptide to form β-sheet-rich aggregates and induce apoptosis has made amyloid fibrils a leading target for the development of novel pharmacotherapies used in managing and treatment of neuropathological conditions such as AD-related cognitive decline. Additionally, deposits of β-sheets folded amylin, a glucose homeostasis regulator, are also present in diabetic patients. Thus, therapeutic compounds capable of reducing intracellular protein aggregation in models of neurodegenerative disorders may prove useful in ameliorating type 2 diabetes mellitus symptoms. Furthermore, both diabetes and neurodegenerative conditions, such as AD, are characterized by chronic inflammatory responses accompanied by the presence of dysregulated inflammatory biomarkers. This review presents current evidence describing the role of various small bioactive molecules known to ameliorate amyloidosis and subsequent effects in prevention and development of diabetes and AD. It also highlights the potential efficacy of peptide–drug conjugates capable of targeting intracellular targets.

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“…In addition to physical impairments, stroke patients often endure post‐stroke anxiety and cognitive impairment including learning and memory deficit, resulting in significant decline in life quality 2 . Previous studies in rodents reported that both middle cerebral artery occlusion (MCAO) and the bilateral common carotid artery occlusion (BCCAO) induced anxiety‐like behavior and spatial learning and memory impairment 3,4 5,6 …”

Section: Introductionmentioning

confidence: 99%

Progranulin promotes hippocampal neurogenesis and alleviates anxiety‐like behavior and cognitive impairment in adult mice subjected to cerebral ischemia

Sun

Zhou

et al. 2022

CNS Neurosci Ther

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Aims: Cerebral ischemia can lead to anxiety and cognitive impairment due to the loss of hippocampal neurons. Facilitation of endogenous neurogenesis in the hippocampus is a potential therapeutic strategy for alleviating ischemia-induced anxiety and cognitive impairment. Progranulin (PGRN), a secretory glycoprotein, has been reported to have a mitogentic effect on many cell types. However, it is not clear whether PGRN enhances hippocampal neurogenesis and promotes functional recovery.Methods: Adult male C57BL/6 mice were subjected to permanent middle cerebral artery occlusion (pMCAO) and injected intracerebroventricularly with recombinant mouse PGRN 30 min after pMCAO. Anxiety-like behavior was detected by the open field and the elevated plus maze tests, and spatial learning and memory abilities were evaluated by Morris water maze. Neurogenesis was examined by double labeling of BrdU and neural stem cells or neurons markers. For mechanism studies, the level of ERK1/2 and AKT phosphorylation were assessed by western blotting.Results: Progranulin significantly alleviated anxiety-like behavior and spatial learning and memory impairment induced by cerebral ischemia in mice. Consistent with the functional recovery, PGRN promoted neural stem cells (NSCs) proliferation and neuronal differentiation in the dentate gyrus (DG) after cerebral ischemia. PGRN upregulated the expression of phosphorylated ERK1/2 and Akt in the DG after cerebral ischemia.Conclusions: Progranulin alleviates ischemia-induced anxiety-like behavior and spatial learning and memory impairment in mice, probably via stimulation of hippocampal neurogenesis mediated by activation of MAPK/ERK and PI3K/Akt pathways. PGRN might be a promising candidate for coping with ischemic stroke-induced mood and cognitive impairment in clinic.

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Alpinia oxyphylla Miq. and Its Active Compound P-Coumaric Acid Promote Brain-Derived Neurotrophic Factor Signaling for Inducing Hippocampal Neurogenesis and Improving Post-cerebral Ischemic Spatial Cognitive Functions

Cited by 30 publications

References 55 publications

The Effect of Propofol on Hypoxia- and TNF-α-Mediated Brain-Derived Neurotrophic Factor/Tyrosine Kinase Receptor B Pathway Dysregulation in Primary Rat Hippocampal Neurons

The Effect of Propofol on Hypoxia- and TNF-α-Mediated Brain-Derived Neurotrophic Factor/Tyrosine Kinase Receptor B Pathway Dysregulation in Primary Rat Hippocampal Neurons

The Use of Bioactive Compounds in Hyperglycemia- and Amyloid Fibrils-Induced Toxicity in Type 2 Diabetes and Alzheimer’s Disease

Progranulin promotes hippocampal neurogenesis and alleviates anxiety‐like behavior and cognitive impairment in adult mice subjected to cerebral ischemia

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