Brain-derived neurotrophic factor exerts neuroprotective actions against amyloid β-induced apoptosis in neuroblastoma cells

Kim, Jin Hee

doi:10.3892/etm.2014.2033

Cited by 26 publications

(16 citation statements)

References 25 publications

(28 reference statements)

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“…A number of studies have reported that the Bcl-2 family proteins participate in AD, and are associated with cell apoptosis (15,16). In particular, Bcl-2 protein is known to inhibit a variety of apoptotic pathways, and in the majority of cases, Bcl-2 is considered to function through the inhibition of Bax protein (17).…”

Section: B Amentioning

confidence: 99%

Paraptosis triggers mitochondrial pathway-mediated apoptosis in Alzheimer's disease

Jia¹,

Wang²,

Zhang³

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. In previous years, increasing evidence has indicated that paraptosis and mitochondrial-mediated apoptosis may be associated with Alzheimer's disease (AD). However, the association between paraptosis and mitochondrial-mediated apoptosis, and the pathological processes underlying AD, remain elusive. In the present study, the β-amyloid precursor protein gene, and the gene mutations PS1M146L and L286V, were transfected to an SH-SY5Y cell line to establish an AD cell model. Subsequently, an MTT assay was used to examine the cell viability of the AD cell model, while a TUNEL assay was employed to observe the number of positively stained apoptotic cells. Cytoplasmic vacuolization was examined using light microscopy and images were photographed. Furthermore, western blot analysis was utilized to detect the expression of golden biomarkers of the mitochondrial pathway, including Bcl-2 and Bax. The paraptosis inhibitor, cycloheximide, was selected to treat the AD model cells in order to observe the association between paraptosis and mitochondrial-mediated apoptosis. The results indicated that the decrease in the cell viability of the AD cells was initiated at 24 h, as compared with the normal cells (P<0.05). TUNEL-positive stained cells were observed at 48 h, which was later compared with the cell death initiation. In addition, examination of cytoplasmic vacuolization using microscopy indicated that there were a small number of paraptosis cells present at 24 h. The expression levels of Bcl-2 was significantly decreased, while Bax was significantly increased at 48 h. Furthermore, cycloheximide treatment was demonstrated to significantly increase Bcl-2 expression, while decreasing Bax expression (P>0.05). In conclusion, the occurrence of paraptosis was demonstrated in the early pathological stages of AD, which may subsequently damage the mitochondria and trigger mitochondrial pathway-mediated apoptosis. Thus, paraptosis may trigger programmed cell death directly, or indirectly through the regulation of Bcl-2 and Bax protein expression.

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Section: B Amentioning

confidence: 99%

Paraptosis triggers mitochondrial pathway-mediated apoptosis in Alzheimer's disease

Jia¹,

Wang²,

Zhang³

et al. 2015

Experimental and Therapeutic Medicine

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“…One of the pathological features of AD is the loss of a large number of neurons. The predominant underlying mechanism of neuronal loss resulting from AD is apoptosis, and the neuronal apoptosis hypothesis is an important aspect of AD pathogenesis (9). The neurons of the brain are particularly sensitive to apoptotic damage (10).…”

Section: Introductionmentioning

confidence: 99%

Protective effect of paeoniflorin on inflammation and apoptosis in the cerebral cortex of a transgenic mouse model of Alzheimer's disease

Cai

et al. 2016

Molecular Medicine Reports

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Paeoniflorin, the main active component of the peony plant, exerts various pharmacological effects. Recently, research on the effect of paeoniflorin on the nervous system has gained more attention. The aim of the present study was to determine whether paeoniflorin exerts a protective effect that improves Alzheimer's disease (AD) via inflammation and apoptosis in the cerebral cortex of a transgenic mouse model of AD. Transgenic mice were used to construct the model of AD and were treated with paeoniflorin. The Morris water maze test was used to analyze cognitive function in AD mice. The protein expression levels of nuclear factor‑κB, tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6 and caspase‑3 were examined with commercial kits. Expression levels of B‑cell lymphoma 2 (Bcl‑2), Bcl‑2‑associated X protein (Bax), phosphorylated (p)‑Akt and p‑p38 mitogen‑activated protein kinase (p‑p38 MAPK) in AD were evaluated by western blotting. The neuroprotective effects of paeoniflorin significantly improved cognitive function and ameliorated patterns of escape distance and escape latency in AD mice. Furthermore, the effects of paeoniflorin decreased inflammation and caspase‑3 activity, and inhibited cell death via increasing the Bcl‑2/Bax ratio and p‑Akt expression levels, and downregulating p‑p38 MAPK expression in AD mice.

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“…As a member of neurotrophic factor family, which can support the growth, survival, and differentiation of neurons, BDNF has attracted wide attention for its multipotency in diverse brain diseases, whereas its potential regulatory role in ropivacaine-induced neuronal injury was not explored and consequently became the focus of our research [19,20].To further verify the regulatory role of BDNF in this pathological procedure, the ropivacaine-damaged cells were treated with BDNF, showing that under the protection of BDNF, the morphological damages presented by synapse disappearance and cell atrophy were significantly reversed, which preliminarily indicates its protective role in ropivacaine-induced neuronal injury at the cytological level. Similar phenomena have also been observed in various related studies [21].…”

Section: Discussionmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor Alleviates Ropivacaine-Induced Neuronal Damage by Enhancing the Akt Signaling Pathway

Zhai

Liu

et al. 2019

Med Sci Monit

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Departmental sources Background: Brain-derived neurotrophic factor (BDNF) is one of the neurotrophic factors that modulate critical metabolic activities, including apoptosis, proliferation, and differentiation modulation. Although numerous studies have focused on the damaging effects of BDNF on neurons, the underlying relationship between these effects remains unclear. In the present study, we investigated the protective effect of BDNF on neuronal injury induced by ropivacaine and assessed whether it is related to the Akt signaling pathway. Material/Methods: Human neuroblastoma cell line SH-SY5Y cells were stimulated with ropivacaine at different concentrations to induce neuronal injury. MTT analysis, flow cytometry, immunohistochemistry, qRT-PCR, and Western blot were used to investigate the proliferation activity, apoptotic level, and expression of Akt, PCNA, Bax, Bcl-2, and cleaved caspase-3, collectively demonstrating the underlying regulatory mechanisms. Results: Compared with the control group, the morphological damage and proliferation inhibition of SH-SY5Y cells induced by ropivacaine were dose-dependent and time-dependent, accompanied by a significant decrease in Akt expression. We treated cells with BDNF or SC79, which is a selective cell-permeable small molecule Akt activator. The results showed that, compared to the ropivacaine group, the morphological damage of neurons was alleviated; cell proliferation activity was enhanced; apoptotic rate was reduced; PCNA, Bcl-2, and phosphorylated Akt expression levels were increased; and Bax and caspase-3 gene and protein expression were decreased. We were able to reverse these effects by administering API-2, an Akt inhibitor. Conclusions: BDNF can alleviate ropivacaine-induced neuronal injury by activating Akt signaling pathway, consequently modulating the proliferation and apoptosis of neurons.

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Brain-derived neurotrophic factor exerts neuroprotective actions against amyloid β-induced apoptosis in neuroblastoma cells

Cited by 26 publications

References 25 publications

Paraptosis triggers mitochondrial pathway-mediated apoptosis in Alzheimer's disease

Paraptosis triggers mitochondrial pathway-mediated apoptosis in Alzheimer's disease

Protective effect of paeoniflorin on inflammation and apoptosis in the cerebral cortex of a transgenic mouse model of Alzheimer's disease

Brain-Derived Neurotrophic Factor Alleviates Ropivacaine-Induced Neuronal Damage by Enhancing the Akt Signaling Pathway

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