Memantine, NMDA Receptor Antagonist, Attenuates ox-LDL-Induced Inflammation and Oxidative Stress via Activation of BDNF/TrkB Signaling Pathway in HUVECs

Hao, Ying; Xiong, Rui; Gong, Xue

doi:10.1007/s10753-020-01365-z

Cited by 22 publications

(12 citation statements)

References 29 publications

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“…Consistently, a decrease in BDNF levels has been reported in neurodegenerative disorders, such as AD [69,71], Huntington's disease (HD) [72], and epilepsy [73], and recent strategies aimed at sustaining or even amplifying the production of BDNF have been proved to be beneficial in patients with HD [74], AD [75,76], Parkinson's disease (PD) [77,78], amyotrophic lateral sclerosis (ALS) [79][80][81], stroke [82][83][84], and spinal cord injury [85][86][87][88]. However, it is worth mentioning that despite the extensive literature dating back to the early 1990s, in which reduced BDNF levels in the brain have been associated with neurodegenerative diseases, only in patients with HD has a genetic defect in BDNF gene been mechanistically related to the pathology [89].…”

Section: Bdnf In Health and Diseasementioning

confidence: 84%

Putting Cells in Motion: Advantages of Endogenous Boosting of BDNF Production

Brattico

Bonetti

Ferretti

et al. 2021

Cells

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Motor exercise, such as sport or musical activities, helps with a plethora of diseases by modulating brain functions in neocortical and subcortical regions, resulting in behavioural changes related to mood regulation, well-being, memory, and even cognitive preservation in aging and neurodegenerative diseases. Although evidence is accumulating on the systemic neural mechanisms mediating these brain effects, the specific mechanisms by which exercise acts upon the cellular level are still under investigation. This is particularly the case for music training, a much less studied instance of motor exercise than sport. With regards to sport, consistent neurobiological research has focused on the brain-derived neurotrophic factor (BDNF), an essential player in the central nervous system. BDNF stimulates the growth and differentiation of neurons and synapses. It thrives in the hippocampus, the cortex, and the basal forebrain, which are the areas vital for memory, learning, and higher cognitive functions. Animal models and neurocognitive experiments on human athletes converge in demonstrating that physical exercise reliably boosts BDNF levels. In this review, we highlight comparable early findings obtained with animal models and elderly humans exposed to musical stimulation, showing how perceptual exposure to music might affect BDNF release, similar to what has been observed for sport. We subsequently propose a novel hypothesis that relates the neuroplastic changes in the human brains after musical training to genetically- and exercise-driven BDNF levels.

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Section: Bdnf In Health and Diseasementioning

confidence: 84%

Putting Cells in Motion: Advantages of Endogenous Boosting of BDNF Production

Brattico

Bonetti

Ferretti

et al. 2021

Cells

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“…It is known that BDNF/TrkB dysregulation was correlated with several vicious factors, such as oxidative stress and in ammation [27]. In the current study we focused on two factors (hypoxia and in ammation) which are major stimuli during the development of neurological disorders, and two cell types (hippocampal neurons and astrocytes) which are major sources of BDNF in CNS.…”

Section: Discussionmentioning

confidence: 99%

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

Tao

Ding

et al. 2021

Preprint

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Background: 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 exposed to hypoxia or TNF-α.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 phosphorylaion of ERK (p-ERK) and CREB at Ser142 (p-CREBSer142), while reduced the phosphorylation of CREB at Ser133 (p-CREBSer133), which were all reversed by 25μM propofol and 10μM ERK inhibitor. In addition, 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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“…It has been shown that NMDA receptors mediated an oxidative stress in neurons [51]. In this regard, it has been determined that NMDA receptor antagonists prevent the oxidative stress biomarkers [15].…”

Section: Discussionmentioning

confidence: 99%

NMDA Receptor Mediates the Anticonvulsant Effect of Hydroalcoholic Extract of Artemisia persica in PTZ-Induced Seizure in Mice

Boroujeni

Lorigooini

Piroti

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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It is necessary to seek more effective sources to design new drug against epilepsy. This study aimed to evaluate the effect of hydroalcoholic extract of Artemisia persica on pentylenetetrazole- (PTZ-) induced seizure in male mice by investigating the possible role of the NMDA receptor and antioxidative stress effect. The phenolic profile of A. persica extract was determined by HPLC-DAD analysis. Mice were treated with normal saline or A. persica extract or pentobarbital or a subeffective dose of extract plus ketamine (NMDA receptor antagonist) and/or effective dose of extract plus NMDA. PTZ (90 mg/kg) was injected intravenously for induction of seizure. The seizure threshold was measured. Then mice were euthanized and the antioxidant capacity and the level of malondialdehyde (MDA) of the prefrontal cortex and serum were measured. The gene expression of NMDA receptor subunits (Nr2a and Nr2b) was determined by real-time PCR. Findings showed that A. persica extract increased the seizure threshold, increased antioxidant capacity, and decreased MDA levels in the serum and brain samples. A. persica extract reduced the expression of NMDA receptor subunits. The result showed that ketamine potentiated the effect of the subeffective dose of extract. HPLC analysis showed that quercetin had the highest flavonoid content and also caffeic acid had the highest content of the phenolic acids. A. persica extract probably via NMDA receptor exerts anticonvulsant properties.

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Memantine, NMDA Receptor Antagonist, Attenuates ox-LDL-Induced Inflammation and Oxidative Stress via Activation of BDNF/TrkB Signaling Pathway in HUVECs

Cited by 22 publications

References 29 publications

Putting Cells in Motion: Advantages of Endogenous Boosting of BDNF Production

Putting Cells in Motion: Advantages of Endogenous Boosting of BDNF Production

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

NMDA Receptor Mediates the Anticonvulsant Effect of Hydroalcoholic Extract of Artemisia persica in PTZ-Induced Seizure in Mice

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