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Source: Journal of Molecular Neuroscience

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Total 63 results found since Jan 2013.

Curcumin Alleviates β Amyloid-Induced Neurotoxicity in HT22 Cells via Upregulating SOD2
In this study, the HT22 neuronal cells were exposed to Aβ to imitate neuronal injury in Alzheimer’s disease (AD). After 24-h treatment, 10 μM Aβ decreased cell viability and mitochondrial functions, including mitochondrial complex activities and mitochondrial membrane potential (MMP), and also downregulated anti-oxidants SOD2, glutathione (GSH), and catalase (CAT) levels (P <  0.05), meanwhile, increased lactic dehydrogenase (LDH) release, apoptosis level, intracellular reactive oxygen species (ROS) and mitochondrial superoxide accumulation (P <  0.05). And, co-administration of 1 μM curcumin signific...
Source: Journal of Molecular Neuroscience - February 12, 2019 Category: Neuroscience Source Type: research

Effects of NLRP6 in Cerebral Ischemia/Reperfusion (I/R) Injury in Rats
AbstractThe NOD-like receptor protein 6 (NLRP6), an intracytoplasmic pattern recognition receptor in the nucleotide-binding domain, leucine-rich repeat-containing (NLR) innate immune receptor family, influences the inflammation reaction. The role of NLRP6 in cerebral ischemia-reperfusion (I/R) injury in rats is unclear. We explore the function of NLRP6 in cerebral I/R injury. The investigators used a middle cerebral artery occlusion/reperfusion model (MCAO) to imitate ischemic injury. We found the peak expression of NLRP6 is in 48-h post-cerebral I/R injury. The expression of NLRP6 siRNA, as well as the expression of prote...
Source: Journal of Molecular Neuroscience - July 1, 2019 Category: Neuroscience Source Type: research

Role of Metallothionein-1 and Metallothionein-2 in the Neuroprotective Mechanism of Sevoflurane Preconditioning in Mice
This study investigated the protective effects and mechanisms of sevoflurane preconditioning (SPC) on neurons in ischemic mice. After SPC, mice were subjected to middle cerebral artery occlusion (MCAO). Cerebral infarction area, cell apoptosis, and metallothionein-1 (MT-1) and metallothionein-2 (MT-2) expressions in MCAO mice were analyzed. Mouse primary neurons were isolated and cultured to determine the location of metallothioneins (MTs) using immunofluorescence. Neurons transfected with MT-siRNA, exogenous MTs, or sh-MTF-1 were subjected to SPC and/or oxygen-glucose deprivation (OGD), and MT-1/MT-2 expression and neurot...
Source: Journal of Molecular Neuroscience - January 16, 2020 Category: Neuroscience Source Type: research

Interleukin Enhancer Binding Factor 2 Regulates Cell Viability and Apoptosis of Human Brain Vascular Smooth Muscle Cells
This study was aimed to explore the effects ofILF2 on IA progression. Human brain VSMCs (hBVSMCs) were transfected with pCDNA3.1(+), pCDNA3.1(+)-ILF2, siRNA-negative control, and siRNA-ILF2. The transfection efficiency was then evaluated by determiningILF2 expression. The cell viability and apoptosis were determined using Cell Counting Kit-8 and Annexin V-FITC cell apoptosis assay kit, respectively. Real-time quantification PCR (RT-qPCR) was applied to measure the expression levels of apoptosis-related and inflammation-related genes. Finally, western blot was used to detect the expression level of Fas cell surface death re...
Source: Journal of Molecular Neuroscience - August 3, 2020 Category: Neuroscience Source Type: research

c-Abl Tyrosine Kinase-Mediated Neuronal Apoptosis in Subarachnoid Hemorrhage by Modulating the LRP-1-Dependent Akt/GSK3 β Survival Pathway
AbstractAccumulating evidence suggests that neuronal apoptosis plays a critical role in early brain injury (EBI) after subarachnoid hemorrhage (SAH), and the inhibition of apoptosis can induce neuroprotective effects in SAH animal models. c-Abl has been reported to promote neuronal apoptosis in Alzheimer ’s disease and cerebral ischemia, but its role in SAH had not been illuminated until now. In the present study, the effect of c-Abl on neuronal apoptosis induced by SAH was investigated. c-Abl protein levels and neuronal apoptosis were markedly increased 24 h after SAH, and the inhibition of endo genous c-Abl reduced ne...
Source: Journal of Molecular Neuroscience - November 19, 2021 Category: Neuroscience Source Type: research

Metabolism-related MOGS Gene is Dysregulated After Peripheral Nerve Injury and Negatively Regulates Schwann Cell Plasticity
AbstractCellular metabolism is essentially linked to tissue remodeling and organ regeneration.MOGS, a gene that encodes cellular metabolism-related protein mannosyl-oligosaccharide glucosidase, was found to be upregulated in nerve segments after peripheral nerve injury. Bioinformatic analyses identified upstream regulators of MOGS and MOGS-associated genes and indicated the significant involvement of cellular metabolism in peripheral nerve regeneration. Functional assessment showed that siRNA-mediated knockdown of MOGS led to elevated proliferation, migration, and differentiation of Schwann cells, indicating the negative r...
Source: Journal of Molecular Neuroscience - May 16, 2022 Category: Neuroscience Source Type: research

miR-134 Regulates Ischemia/Reperfusion Injury-Induced Neuronal Cell Death by Regulating CREB Signaling
Abstract microRNA-134 (miR-134) has been reported to be a brain-specific miRNA and is differently expressed in brain tissues subjected to ischemic injury. However, the underlying mechanism of miR-134 in regulating cerebral ischemic injury remains poorly understood. The current study was designed to delineate the molecular basis of miR-134 in regulating cerebral ischemic injury. Using the oxygen-glucose deprivation (OGD) model of hippocampal neuron ischemia in vitro, we found that the overexpression of miR-134 mediated by recombinant adeno-associated virus (AAV) vector infection significantly promoted neuron death ...
Source: Journal of Molecular Neuroscience - October 16, 2014 Category: Neuroscience Source Type: research

Upregulated Expression of Ebp1 Contributes to Schwann Cell Differentiation and Migration After Sciatic Nerve Crush
Abstract Ebp1, an ErbB3-binding protein, is the human homologue of the cell cycle-regulated mouse protein p38-2G4. Ebp1 was reported to inhibit the proliferation and induce the differentiation of human cancer cells. Its p48 isoform contributes to neuronal differentiation and growth factor specificity. However, the expression and role of Ebp1 in peripheral system lesions and repair are still unknown. Herein, we investigated the spatiotemporal pattern of Ebp1 expression following sciatic nerve crush. After crush, the level of Ebp1 protein was elevated gradually, peaked at day 5, and then declined to the normal at ...
Source: Journal of Molecular Neuroscience - November 27, 2014 Category: Neuroscience Source Type: research

The Expression of CAP1 After Traumatic Brain Injury and Its Role in Astrocyte Proliferation
Abstract Adenylate cyclase-associated protein 1 (CAP1), a member of cyclase-associated proteins involved in the regulation of actin filaments, was recently reported to play a role in the pathology of sciatic nerves injury. However, the distribution and function of CAP1 in the central nervous system (CNS) remain unclear. To investigate whether CAP1 is involved in CNS injury and repair, we used an acute traumatic brain injury (TBI) model in adult rats. Western blot analysis and immunohistochemistry showed a significant upregulation of CAP1 in ipsilateral peritrauma cortex compared with the contralateral and sham-op...
Source: Journal of Molecular Neuroscience - December 1, 2014 Category: Neuroscience Source Type: research

Nucleolin Promotes TGF-β Signaling Initiation via TGF-β Receptor I in Glioblastoma
In conclusion, nucleolin promotes and regulates the TGF-β pathway by interacting with TβR-I and is required for initiation and activation of TGF-β signaling. Thus, nucleolin could be a key factor in glioblastoma pathogenesis and considered a therapeutic target, which may also mediate more signaling pathways.
Source: Journal of Molecular Neuroscience - January 1, 2015 Category: Neuroscience Source Type: research

FRK Inhibits Migration and Invasion of Human Glioma Cells by Promoting N-cadherin/β-catenin Complex Formation
In this study, we found that FRK over-expression increased the protein level of N-cadherin, but not E-cadherin. Meanwhile, FRK over-expression promoted β-catenin translocation to the plasma membrane, where it formed complex with N-cadherin, while decreased β-catenin level in the nuclear fraction. In addition, down-regulation of N-cadherin by siRNA promoted the migration and invasion of glioma U251 and U87 cells and abolished the inhibitory effect of FRK on glioma cell migration and invasion. In summary, these results indicate that FRK inhibits migration and invasion of human glioma cells by promoting N-cadherin/β-catenin complex formation.
Source: Journal of Molecular Neuroscience - January 1, 2015 Category: Neuroscience Source Type: research

Involvement of Nrf2 in Development of Anxiety-Like Behavior by Linking Bcl2 to Oxidative Phosphorylation: Estimation in Rat Hippocampus, Amygdala, and Prefrontal Cortex
In this study, we evaluated whether silencing of Nrf2 plays a role in development of anxiety-related behavior. In this regard, we exerted small interfering RNA (siRNA) targeting Nrf2 in dorsal third ventricle and subsequently examined the effect of this silencing on anxiety-related behavior along with supposed molecular mechanisms. Therefore, we evaluated apoptotic markers and mitochondrial electron transport chain (ETC) activity in three brain regions: hippocampus, amygdala, and prefrontal cortex. Based on our result, Nrf2-silenced rats exhibited greater anxiety-like behavior compared to control group. Furthermore, Nrf2 s...
Source: Journal of Molecular Neuroscience - January 23, 2015 Category: Neuroscience Source Type: research

Wogonin Induced Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Human Malignant Neuroblastoma Cells Via IRE1α-Dependent Pathway
Abstract Wogonin, a flavonoid isolated from Scutellaria baicalensis Georgi, has been reported to exhibit a variety of biological effects including anti-cancer effects. It has a pro-apoptotic role in many cancer types. However, the molecular mechanisms of wogonin in treating neuroblastoma remain elusive. In the present study, two malignant neuroblastoma cell lines (SK-N-BE2 and IMR-32 cells) were treated with different doses of wogonin (0–150 μM). Wogonin showed significant cytotoxic effects in SK-N-BE2 and IMR-32 cells in a dose- and time-dependent manner. Treatment of SK-N-BE2 and IMR-32 cells with 75 μΜ w...
Source: Journal of Molecular Neuroscience - March 5, 2015 Category: Neuroscience Source Type: research