Ethanol exposure disrupted the formation of radial glial processes and impaired the generation and migration of outer radial glial cells in forebrain organoids derived from human embryonic stem cells.

Radial glial cells (RGCs) play a pivotal role in cerebral cortical development by functioning as a source of new neurons and by supporting the migration of newborn neurons. These functions are primarily dependent on the apical-basolateral structures of radial glial processes. This study aims to investigate the effects of ethanol exposure on the development of radial glial processes and the generation, migration, and transformation of outer radial glial cells (oRGCs).

Up-regulation of microRNA-34a mediates ethanol-induced impairment of neural crest cell migration in vitro and in zebrafish embryos through modulating epithelial-mesenchymal transition by targeting Snail1.

Prenatal ethanol exposure can impair neural crest cell (NCC) development, including NCC survival, differentiation and migration, contributing to the craniofacial dysmorphology in Fetal Alcohol Spectrum Disorders (FASD). Epithelial-mesenchymal transition (EMT) plays an important role in regulating the migration of NCCs. The objective of this study is to determine whether ethanol exposure can suppress NCC migration through inhibiting EMT and whether microRNA-34a (miR-34a) is involved in the ethanol-induced impairment of EMT in NCCs.

Porphyromonas gingivalis infection exacerbates oesophageal cancer and promotes resistance to neoadjuvant chemotherapy.

Background: The effect of Porphyromonas gingivalis (Pg) infection on oesophageal squamous cell carcinoma (ESCC) prognosis, chemotherapeutic efficacy, and oesophageal cancer cell apoptosis resistance and proliferation remain poorly understood.

Methods: Clinicopathological data from 312 ESCC oesophagectomy patients, along with the computed tomography imaging results and longitudinal cancerous tissue samples from a patient subset (n = 85) who received neoadjuvant chemotherapy (NACT), were analysed. Comparison of overall survival and response rate to NACT between Pg-infected and Pg-uninfected patients was made by multivariate Cox analysis and Response Evaluation Criteria in Solid Tumours v.

Sulforaphane Protects Against Ethanol-Induced Apoptosis in Human Neural Crest Cells Through Diminishing Ethanol-Induced Hypermethylation at the Promoters of the Genes Encoding the Inhibitor of Apoptosis Proteins.

The neural crest cell (NCC) is a multipotent progenitor cell population that is sensitive to ethanol and is implicated in the Fetal Alcohol Spectrum Disorders (FASD). Studies have shown that sulforaphane (SFN) can prevent ethanol-induced apoptosis in NCCs. This study aims to investigate whether ethanol exposure can induce apoptosis in human NCCs (hNCCs) through epigenetically suppressing the expression of anti-apoptotic genes and whether SFN can restore the expression of anti-apoptotic genes and prevent apoptosis in ethanol-exposed hNCCs.

MicroRNA-135a Protects Against Ethanol-Induced Apoptosis in Neural Crest Cells and Craniofacial Defects in Zebrafish by Modulating the Siah1/p38/p53 Pathway.

MicroRNAs (miRNAs) are small non-coding RNAs that are involved in various biological processes, including apoptosis, by regulating gene expression. This study was designed to test the hypothesis that ethanol-induced downregulation of miR-135a contributes to ethanol-induced apoptosis in neural crest cells (NCCs) by upregulating Siah1 and activating the p38 mitogen-activated protein kinase (MAPK)/p53 pathway. We found that treatment with ethanol resulted in a significant decrease in miR-135a expression in both NCCs and zebrafish embryos.

Oxysophocarpine reduces oxidative stress and inflammation in tuberculosis-infected neutrophils and mouse lungs.

Tuberculosis (TB) is a chronic inflammatory infectious disease caused by (Mtb), which induces irreversible pulmonary damage. Oxysophocarpine (OSC) is a natural alkaloid that exhibits multiple pharmacological activities, including anti-inflammation; however, the protective effects of OSC against TB and the mechanisms involved are unknown. Here, we established murine and cellular models of TB with C3HeB/FeJ mice and neutrophils infected with H37Rv to investigate the biological functions of OSC in TB.

JAK3 restrains inflammatory responses and protects against periodontal disease through Wnt3a signaling.

Homeostasis between pro- and anti- inflammatory responses induced by bacteria is critical for the maintenance of health. In the oral cavity, pro-inflammatory mechanisms induced by pathogenic bacteria are well-established; however, the anti-inflammatory responses that act to restrain innate responses remain poorly characterized. Here, we demonstrate that infection with the periodontal pathogen Porphyromonas gingivalis enhances the activity of Janus kinase 3 (JAK3) in innate immune cells, and subsequently phospho-inactivates Nedd4-2, an ubiquitin E3 ligase.

Sulforaphane protects against ethanol-induced apoptosis in neural crest cells through restoring epithelial-mesenchymal transition by epigenetically modulating the expression of Snail1.

Ethanol-induced apoptosis in neural crest cells (NCCs), a multipotent progenitor cell population, is implicated in the Fetal Alcohol Spectrum Disorders (FASD). Studies have demonstrated that sulforaphane (SFN) can prevent ethanol-induced apoptosis in NCCs. The objective of this study is to investigate whether ethanol exposure can induce apoptosis in NCCs by inhibiting epithelial-mesenchymal transition (EMT) and whether SFN can prevent ethanol-induced apoptosis by epigenetically modulating the expression of Snail1, a key transcriptional factor that promotes EMT.

MicroRNA-34a mediates ethanol-induced impairment of neural differentiation of neural crest cells by targeting autophagy-related gene 9a.

Neural crest cells (NCCs) are multipotent progenitor cells that are sensitive to ethanol and are implicated in Fetal Alcohol Spectrum Disorders (FASD). The objective of this study is to test whether ethanol exposure can inhibit the neural differentiation of NCCs by inhibiting autophagy and whether miR-34a is involved in ethanol-induced inhibition of autophagy in NCCs. We found that ethanol exposure resulted in the inhibition of neural differentiation of NCCs.

Decreased expression of ubiquilin‑1 following neonatal hypoxia‑ischemic brain injury in mice.

Ubiquilin‑1 (Ubqln), a ubiquitin‑like protein, regulates degradation of misfolded proteins and has been reported to have a crucial role in multiple pathologic and physiologic conditions. The current study was undertaken to investigate the expression of Ubqln in the brain of a neonatal hypoxia‑ischemic (HI) brain injury model induced using the Rice method with some modifications. Mouse pups at postnatal day 7 day were used in this study.

The novel targets of DL-3-n-butylphthalide predicted by similarity ensemble approach in combination with molecular docking study.

Background: DL-3-n-butylphthalide (NBP) is a drug for treating acute ischemic stroke, and may play a neuroprotective role by acting on multiple active targets. The aim of this study was to predict the target proteins of NBP in mammalian cells.

Methods: The similarity ensemble approach search tool (SEArch), one of the commonly used public bioinformatics tools for target prediction, was employed in the experiment.

Niche astrocytes promote the survival, proliferation and neuronal differentiation of co-transplanted neural stem cells following ischemic stroke in rats.

Niche astrocytes have been reported to promote neuronal differentiation through juxtacrine signaling. However, the effects of astrocytes on neuronal differentiation following ischemic stroke are not fully understood. In the present study, transplanted astrocytes and neural stem cells (NSCs) were transplanted into the ischemic striatum of transient middle cerebral artery occlusion (MCAO) model rats 48 h following surgery.

USP14 inhibitor attenuates cerebral ischemia/reperfusion-induced neuronal injury in mice.

Stroke is associated with over-production of misfolded and aggregating proteins. However, it remains largely unclear whether enhanced removal of protein aggregates following ischemic stroke is neuroprotective. Deubiquitinating enzymes (DUBs) are a large group of proteases that regulate protein degradation.

Overexpression of β-Catenin Induces Cisplatin Resistance in Oral Squamous Cell Carcinoma.

Abnormal expression of β-catenin contributes to tumor development, progression, and metastasis in various cancers. However, little is known about the relationship between abnormal expression of β-catenin and cisplatin chemotherapy in oral squamous cell carcinoma (OSCC). The present study aimed to investigate the effect of β-catenin on OSCC cisplatin resistance and evaluated the drug susceptibility of stable cell lines with β-catenin knockin and knockdown.

Dissociation of E-cadherin/β-catenin complex by MG132 and bortezomib enhances CDDP induced cell death in oral cancer SCC-25 cells.

E-cadherin/β-catenin complex plays an important role in maintaining the homeostasis of tissues and regulating cell proliferation, survival and apoptosis. To address the relationships between the change of E-cadherin/β-catenin complex and cell apoptosis, human oral squamous carcinoma SCC-25 cells were used to investigate whether the dissociation of the E-cadherin/β-catenin complex was the main reason of MG132- or bortezomib-induced apoptosis. We found that MG132 or bortezomib alone induced remarkable loss of cell integrity and contact, inhibited cell growth, survival, migration and caused cell cycle arrest, intracellular ROS production.

Effects of hypoxia on progranulin expression in HT22 mouse hippocampal cells.

The present study evaluated the effect of hypoxia on the expression of progranulin in HT22 mouse hippocampal cells. To investigate progranulin (PGRN) and the alterations in its expression following hypoxia, the HT22 cells were treated with various concentrations of sodium hydrosulfite (Na2S2O4; 1-20 mM) for a fixed time (6 h) or with a fixed concentration (5 mM) for different lengths of time (2-0 h). The expression of PGRN in the HT22 cells following hypoxia was analyzed by an immunocytochemistry assay and western blot analysis.

Ubiquilin-1 protects cells from oxidative stress and ischemic stroke caused tissue injury in mice.

Ubiquilin-1 (Ubqln1 or Ubqln), a ubiquitin-like protein, mediates degradation of misfolded proteins and has been implicated in a number of pathological and physiological conditions. To better understand its function in vivo, we recently generated transgenic (Tg) mice that globally overexpress mouse Ubqln in a variety of tissues and ubqln conditional knock-out mice. The Tg mice were viable and did not show any developmental or behavioral abnormalities compared with their wild-type (WT) littermates.

Progranulin expression in neural stem cells and their differentiated cell lineages: an immunocytochemical study.

Progranulin (PGRN) is a neurotrophic factor that regulates neurite outgrowth and enhances neuronal survival. The association between PGRN and neural stem cell (NSC) differentiation may aid in elucidating the underlying pathogenesis and potential treatments for neurodegenerative diseases. To investigate the association between PGRN and NSCs and their lineages, primary NSCs were prepared from the subventricular zone of neonatal Sprague Dawley pups (age, 1 day) and cultured in the neural stem cell medium.

Transient focal cerebral ischemia upregulates immunoproteasomal subunits.

This study was designed to determine whether focal cerebral ischemia alters the expression of the immunoproteasomal (i-proteasomal) subunits. Transient cerebral ischemia significantly increased the expression of the i-proteasomal subunits, 20S β1i (LMP2) and β5i (LMP7) in the parietal cortex and hippocampus. This alteration was associated with a remarkable increase in ubiquitinated proteins.

Exocytosis of MTT formazan could exacerbate cell injury.

MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] method is one of the most widely used methods to analyze cell proliferation and viability. It is taken up through endocytosis and is reduced by mitochondrial enzymes as well as endosomal/lysosomal compartments, then is transported to cell surfaces to form needle-like MTT formazans; however the effect of MTT itself still remains elusive. Our objective was to investigate the direct effects of MTT on in vitro SH-SY5Y cells.

Effects of DL-3-n-butylphthalide on vascular dementia and angiogenesis.

3-n-Butylphthalide (NBP) is a compound extracted from Chinese celery and is used as an anti-hypertensive herbal medicine for treating stroke patients. The aim of this study is to demonstrate the effects and mechanisms of this compound through in vitro and in vivo experiments. Culture experiments were performed by adding hydrogen peroxide (H(2)O(2)) to SH-SY5Y cells.

Protective effects and potential mechanisms of Pien Tze Huang on cerebral chronic ischemia and hypertensive stroke.

Background: Stroke caused by brain ischemia is the third leading cause of adult disability. Active prevention and early treatment of stroke targeting the causes and risk factors may decrease its incidence, mortality and subsequent disability. Pien Tze Huang (PZH), a Chinese medicine formula, was found to have anti-edema, anti-inflammatory and anti-thrombotic effects that can prevent brain damage.

The toxic effect of ketamine on SH-SY5Y neuroblastoma cell line and human neuron.

Ketamine used as an injectable anesthetic in human and animal medicine is also a recreational drug used primarily by young adults often at all night dance parties in nightclubs. The percentage of ketamine users has grown very fast in the last 5 years worldwide. However, this leads to the serious question of the long-term adverse effects of ketamine on our nervous system, particularly the brain, because ketamine as an NMDA antagonist could cause neurons to commit apoptosis.

The difference in gliosis induced by β-amyloid and Tau treatments in astrocyte cultures derived from senescence accelerated and normal mouse strains.

Astrocytes react to various neurodegenerative insults rapidly and undergo changes known as gliosis or astrogliosis. In Alzheimer's disease (AD), a wall of reactive astrocytes surrounds senile plaques of β-amyloid (Aβ) and might play an important role in clearing of Aβ. AD is neuropathologically characterized by the co-existence of two pathological structures, senile plaques and neurofibrillary tangles composed of Aβ and Tau protein respectively.

Pien Tze Huang, a composite Chinese traditional herbal extract, affects survival of neuroblastoma cells.

Pien Tze Huang is a popular Chinese medicine for liver diseases. In the investigations of possible effects of Pien Tze Huang on the central nervous system, we first studied the in vitro anti-cancer activity of Pien Tze Huang on neuroblastoma cells (SH-SY5Y) as compared with normal fibroblasts (NIH-3T3). Results showed that Pien Tze Huang significantly decreased (p < .