جستجوی مقالات مرتبط با کلیدواژه "neuron" در نشریات گروه "پزشکی"

Spinal cord injury (SCI) is a complex, multifaceted, progressive, and yet incurable complication that can cause irreversible damage to the individual, family, and society. In recent years strategies for the management and rehabilitation of SCI besides axonal regeneration, remyelination, and neuronal plasticity of the injured spinal cord have significantly improved. Although most of the current research and therapeutic advances have been made in animal models, so far, no specific and complete treatment has been reported for SCI in humans. The failure to treat this complication has been due to the inherent neurological complexity and the structural, cellular, molecular, and biochemical characteristics of spinal cord injury. In this review, in addition to elucidating the causes of spinal cord injury from a molecular and pathophysiological perspective, the complexity and drawbacks of neural regeneration that lead to the failure in SCI treatment are described. Also, recent advances and cutting -edge strategies in most areas of SCI treatment are presented.  Level of evidence: I

Human umbilical cord mesenchymal stem cells (hUMSCs) have been considered to repair damaged tissues and cells. This study aims to investigate the differentiation efficiency affected by Schwann cells (SCs) and laminin and also compare them to other strategies using chemicals or growth factors.

SCs and hUMSCs were separated from dorsal root ganglion of rats and newborn human umbilical cords (hUCs), respectively, and then cultured. The marker expressions of mesenchymal stem cells (MSCs), hematopoietic and endothelial for hUMSCs were confirmed by flow cytometry. The hUMSCs were cultured in four groups: 1) control, 2) co-culture with SCs (C), 3) laminin (L), and 4) co-culture with SCs treated by laminin (CL). The expression of protein and gene-related differentiation NSE, MAP2 and β-tubulin were examined by real-time polymerase chain reaction (PCR) and immunocytochemistry after 12 days.

The flow cytometry analysis revealed high expression of mesenchymal and low expression of hematopoietic and endothelial markers, where the SCs expressed S100 at a high level (97.4%±2.25). The expression of NSE, MAP2 and β-tubulin increased significantly in the C, L and CL groups compared to the control group (P<0.001), where the CL group had the highest expression among the groups [7.59±0.126, 7.87±0.191, 6.36±0.420, respectively, (P<0.01)]. Also, the expression of neural proteins was significantly increased in tested groups in comparison to the control group.

Combined laminin and SCs co-culturing with hUMCSs could be the most effective strategy for neural differentiation

The fate of neural stem/progenitor cells (NS/PCs) is very important in combination therapies for spinal cord injury (SCI). Methylprednisolone (MP) is the main anti-inflammatory drug currently used in the acute phase of SCI. The present study evaluated the differentiation patterns of NS/PCs following exposure to different concentrations of MP. NS/PCs were isolated from ganglionic eminence of mouse embryos. After the second passage, the obtained cells were treated with 0, 5, 10, 15 and 20 μg/ml of MP. The differentiation of the cells in to immature neuroblasts, mature neurons, astrocytes, and oligodendrocytes was assessedusing immunofluorescence assay. Exposure of the NS/PCs to different concentrations of MP increased the production of astrocytes, neuroblasts, and oligodendrocytes, Whileit didn’t have any considerable effect on the production of more mature neurons. In conclusion, MP can change the fate of NS/PCs toward the generation of astrocytes and oligodendrocytes. This effect should be considered in MP+NS/PCs combination therapy strategies.

Spironolactone has produced beneficial effects in animal models of neurodegenerative disorders. However, the underlying mechanisms of this agent on neurons and glia are mostly unknown. Therefore, we aimed to show the effects of spironolactone and fludrocortisone, a mineralocorticosteroid receptor agonist, on neuronal and glial toxicity induced by N-methyl-D-aspartate (NMDA) activation and chloroquine, an autophagy inhibitor, in the cell culture. We exposed the SHSY5Y neuroblastoma and 1321N1 astrocytoma exposed to NMDA (25µM), or chloroquine (40µM) for 24 and 48h to induce neuronal and glial toxicity. Spironolactone (1, 10, and 20µM) or fludrocortisone (300nM) were also added to the cells for 24 and 48h. Cell survival was measured using the MTT assay. Neurons and astrocytes treated with NMDA and spironolactone (1, 10, and 20µM) for 24 and 48h had lower cell death compared with the NMDA-treated group. Moreover, cells treated with NMDA and fludrocortisone for 24 and 48h had higher viability in comparison to the NMDA-treated group. The neuronal cells treated with chloroquine and spironolactone (10 and 20µM) for 24h had higher cell viability compared with the chloroquine group. Chloroquine plus spironolactone (20µM) treatment for 24 and 48h increased cell viability of astrocytes compared with the chloroquine-treated group. Moreover, the treatment of neurons and astrocytes with chloroquine plus fludrocortisone for 24h decreased cell death.  Spironolactone and fludrocortisone protected neurons and astrocytes against NMDA- and chloroquine-induced toxicity. The mechanism of neuronal and glial protective effects of spironolactone possibly related to the inhibition of the mineralocorticosteroids. However, spironolactone might affect other non-mineralocorticoid systems.

Spironolactone has produced beneficial effects in animal models of neurodegenerative disorders. However, the underlying mechanisms of this agent on neurons and glia are mostly unknown. Therefore, we aimed to show the effects of spironolactone and fludrocortisone, a mineralocorticosteroid receptor agonist, on neuronal and glial toxicity induced by N-methyl-D-aspartate (NMDA) activation and chloroquine, an autophagy inhibitor, in the cell culture. We exposed the SHSY5Y neuroblastoma and 1321N1 astrocytoma exposed to NMDA (25µM), or chloroquine (40µM) for 24 and 48h to induce neuronal and glial toxicity. Spironolactone (1, 10, and 20µM) or fludrocortisone (300nM) were also added to the cells for 24 and 48h. Cell survival was measured using the MTT assay. Neurons and astrocytes treated with NMDA and spironolactone (1, 10, and 20µM) for 24 and 48h had lower cell death compared with the NMDA-treated group. Moreover, cells treated with NMDA and fludrocortisone for 24 and 48h had higher viability in comparison to the NMDA-treated group. The neuronal cells treated with chloroquine and spironolactone (10 and 20µM) for 24h had higher cell viability compared with the chloroquine group. Chloroquine plus spironolactone (20µM) treatment for 24 and 48h increased cell viability of astrocytes compared with the chloroquine-treated group. Moreover, the treatment of neurons and astrocytes with chloroquine plus fludrocortisone for 24h decreased cell death. Spironolactone and fludrocortisone protected neurons and astrocytes against NMDA- and chloroquine-induced toxicity. The mechanism of neuronal and glial protective effects of spironolactone possibly related to the inhibition of the mineralocorticosteroids. However, spironolactone might affect other non-mineralocorticoid systems.

Scopolamine can induce amyloid β accumulation, oxidative stress, synaptic loss, and learning/memory deficit as seen in Alzheimer’s disease. Ginkgo biloba extract increases neurogenesis and suppresses the happening of pathological processes and cognitive decline.

Herein, we explored the effect of Ginkgo biloba extract on scopolamine-induced congophilic amyloid plaque accumulation and neurons density in the rats’ brain.

Ginkgo biloba extract (40 and 80 mg/kg/day) was injected daily intraperitoneally for seven days before and after the scopolamine injection (3 mg/kg) in protective and treatment group rats. At the end of the experiments, the rats’ brains were removed and fixed in 4% paraformaldehyde. After histological processing, Congo red staining was used to assess amyloid plaques while cresyl violet staining was employed to determine the neuron density.

The administration of scopolamine led to increased congophilic amyloid plaque density in the hippocampus and cingulate cortex of the rats. Pretreatment with Ginkgo biloba extract significantly decreased congophilic amyloid plaque numbers in the hippocampus and cingulate cortex. In addition, scopolamine could reduce the hippocampal and cingulate cortex neuron numbers compared to the control group rats. However, Ginkgo biloba extract increased the hippocampal and cingulate cortex neuron numbers before and after the injection of scopolamine.

Our results showed that Ginkgo biloba extract could play protective roles against some scopolamine-induced Alzheimer’s disease-like pathologic dysfunctions, including amyloid β accumulation and neuronal loss, suggesting that treatment with Ginkgo biloba extract might be a promising prophylactic target for Alzheimer’s disease.

To reach an evidence-based knowledge in the context of the temporal-spatial pattern of neuronal death and find appropriate time of intervention in order to preserve spared neurons and promote regeneration after traumatic spinal cord injury (TSCI).
The study design was based on Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA)-guided systematic review. PubMed and EMBASE were searched (24 October, 2015) with no temporal or linguistic restrictions. Hand-search was performed in the bibliographies of relevant articles. Non-interventional animal studies evaluating time-dependent neuronal death following acute mechanical trauma to the spinal cord were included. We separately evaluated the fate of various populations of neurons including propriospinal neurons, ventral motor neurons, Clarke’s column neurons, and supraspinal neurons.
We found 11,557 non-duplicated studies. Screening through the titles and abstracts led to 549 articles, 49 of which met the inclusion criteria. Both necrotic and apoptotic neuronal deaths occur after TSCI, though necrosis is the prominent mechanism. There are differences in the responses of intrinsic neurons of the spinal cord to the TSCI. Also, the extent of neuronal death in the supraspinal neurons depends on the anatomical location of their axons.
In order to develop new therapies, selection of the injury model and time of intervention has a crucial role in the efficacy of therapy. In addition, examining the safety and efficacy of an intervention by reliable methods not confounded by the injury-related changes would promote translation of therapies to the clinical application.

This study aimed to isolate and culture SADS cells, investigate their neurogenic capacity and evaluate their application for nerve tissue engineering.
In this experimental study, SADS cells were isolated from human adipose tissue. After 7-day treatment of SADS cells with insulin, indomethacin and isobutylmethylxanthine, neurogenic differentiation of SADS cells was investigated. During this study, Poly (ε-caprolactone) (PCL) and PCL/gelatin nanofibrous scaffolds were fabricated using electrospinning and subsequently nanofibrous scaffolds were coated with platelet-rich plasma (PRP). SADS cells were also seeded on nanofibrous scaffolds and neurogentic differentiation of these cells on nanofibers was also evaluated. Effect of PRP
on proliferation and differentiation of SADS cells on scaffolds was also studied.
Our results showed that after 7-day treatment of SADS cells with insulin, indomethacin and isobutylmethylxanthine, SADS cells expressed markers characteristic of neural cells such as nestin and neuron specific nuclear protein (NEUN) (as early neuronal markers) as well as microtubule-associated protein 2 (MAP2) and neuronal microtubule-associated (TAU) (as mature neuronal markers) while mature astrocyte maker (GFAP) was not expressed. MTT assay and SEM results showed that incorporation of gelatin and PRP into the structure of nanofibrous scaffolds has a significant positive influence on the bioactivity of scaffolds. Our results also showed neurogentic differentiation of SADS cells on scaffolds.
Our results demonstrated that SADS cells have potential to differentiate into early and mature progenitor neurons, in vitro. PCL/gelatin/PRP was found to be a promising substrate for proliferation of SADS cells and differentiation of these cells into neural cells which make these scaffolds a candidate for further in vivo experiments and suggest their application for nerve tissue engineering.

Passive CLARITY is a whole-tissue clearing protocol, based on sodium dodecyl sulfate (SDS) clearing, for imaging intact tissue containing transgenic or immunolabeled fluorescent proteins. In this study, we present an improved passiveCLARITY protocol with efficient immunolabeling without the need for electrophoresis or complex instrumentation.
In this experimental study, after perfusion of C57BL/6N mice with phosphate-buffered saline (PBS) and then with acrylamide-paraformaldehyde (PFA), the quadriceps femoris muscle was removed. The muscle samples were post-fixed and degassed to initiate polymerization. After removing the excess hydrogel around the muscle, lipids were washed out with the passive CLARITY technique. The transparent whole intact muscles were labeled for vessel and neuron markers, and then imaged by confocal microscopy. Three-dimensional images were reconstructed to present the muscle
tissue architecture.
We established a simple clearing protocol using wild type mouse muscle and labeling of vasculatures and neurons. Imaging the fluorescent signal was achieved by protein fixation, adjusting the pH of the SDS solution and using an optimum temperature (37˚C) for tissue clearing, all of which contributed to the superiority of our protocol.
We conclude that this passive CLARITY protocol can be successfully applied to three-dimensional cellular and whole muscle imaging in mice, and will facilitate structural analyses and connectomics of large assemblies of muscle cells, vessels and neurons in the context of three-dimensional systems.

Improvement of neurologic outcome in progesterone-administered patients with diffuse axonal injury (DAI) has been found in a recent study. Also, there has been interest in the importance of serum parameters as predictors of outcome in traumatic brain injury..
The aim of this study was to examine the effect of progesterone administration on serum levels of neuron-specific enolase (NSE), and intercellular adhesion molecule-1 (ICAM-1) in clinical DAI..
Patients and In this study, the serum levels of ICAM-1 and NSE of 32 male DAI patients (18 - 60 years of age, a Glasgow coma scale of 12 or less, and admitted within 4 hours after injury) who were randomized for a controlled phase II trial of progesterone were analyzed. The analysis was performed between the control and progesterone groups at admission time, and 24 hours and six days after DAI, respectively..
A reduction in the serum level of ICAM-1 was noticed in the progesterone group 24 hours after the injury (P In summary, progesterone administration reduced serum ICAM-1, and whereby may attenuate blood brain barrier disruption, the latter needs further investigation for confirmation..

Cell therapy is a potential therapeutic approach for neurodegenerative disorders. Human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSCs) are an appropriate source of stem cells for use in various cell-based therapies.
In this study, we examined a real-time PCR approach for neural differentiation of hUCB-MSCs in vitro.
MSCs were cultured in DMEM medium supplemented with 10% FBS in a humidified incubator equilibration at 5% CO2 and 37°C. For the neural differentiation of MSCs, the DMEM was removed and replaced with pre-induction media (retinoic acid [RA], basic fibroblast growth factor [bFGF], and epidermal growth factor [EGF]) and basal medium for two days. They were then cultured in nerve growth factor (NGF), 3-isobutyl-1-methylxanthine (IBMX), ascorbic acid (AA), and basal medium for six days. We also monitored the expression of markers for neural differentiation with real-time PCR.
The results of real-time PCR showed that the expression of the GFAP, MBP, and MAP-2 genes after two-step induction was significantly increased compared to the common induction protocol. In addition, our study showed that RA should play the main role in the neural differentiation and fate of MSCs compared to other neural inducers.
Taken together, the combination of chemical and growth factors in the two-step induction protocol may improve the efficiency of MSC differentiation into neural progenitor cells, and may be a new method for the easy and fast application of MSCs in regenerative medicine in the future.