The amyloid precursor protein plus presenilin-1 (APP/PS1) mice are a frequently-used model for Alzheimer’s disease studies (AD). Using behavioral studies, quantitative RT-PCR and Western-blot techniques, significant findings were determined by the expression of proteins involved in inflammation comparing APP/PS1 and Wild type mice. Increased GFAP expression could be associated with the elevation in number of reactive astrocytes. IL-3 is involved in inflammation and ABDF1 intervenes normally in the transport across cell membranes and both were found up-regulated in APP/PS1 mice compared to Wild type mice. We noted for the first time, a CCR8 increase expression with diminution of its CCL1 chemokine, both normally involved in protection from bacterial infection and demyelination. Furthermore, CCR5 expression was decreased and both CCL3 and CCL4 chemokines were highly expressed indicating a possible gliosis and probably an increase in chemotaxis from lymphocytes and T cell generation. Inflammation in AD will be the next step in the therapeutic approach.

Ischemic retinopathy, resulting in multiple lesions like microvasculature damage, inflammation and neovascularization, is a major contributor of vision damage. In these pathological changes, retinal glia cannot be ignored in the development of retinopathy. They constitute a highly versatile population that interacts with various cells to maintain homeostasis and limit disease. Therefore, glial activation and gliosis are strikingly ubiquitous responses to almost every form of retinal disease. Both of microglial cells and Muller cells are major intrinsic retinal glial cells and they are in close relationship, which means they can influence each other, make joint action or even become interdependent. They exhibit morphological and functional changes to have an impact on degree of retinal injury through different responses, which mediated by glial cells are important not only for course of disease progression, but also for the maintenance of neuronal and photoreceptor survival. Thus, defining the mechanisms that underlie communications between microglial cells and Muller cells could enable the development of more selective therapeutic targets, with great potential clinical applications. Key words: Microglia; Muller cell; Review; Ischemic retinopathy

Aβ plaques are one of the two lesions in the brain that define the neuropathological diagnosis of Alzheimer's disease. Plaques are highly diverse structures; many of them include massed, fibrillar polymers of the Aβ protein referred to as Aβ-amyloid, but some lack the defining features of amyloid. Cellular elements in 'classical' plaques include abnormal neuronal processes and reactive glial cells, but these are not present in all plaques. Plaques have been given various names since their discovery in 1892, including senile plaques, amyloid plaques, and neuritic plaques. However, with the identification in the 1980s of Aβ as the obligatory and universal component of plaques, the term 'Aβ plaques' has become a unifying term for these heterogeneous formations. Tauopathy, the second essential lesion of the Alzheimer's disease diagnostic dyad, is downstream of Aβ-proteopathy, but it is critically important for the manifestation of dementia. The etiologic link between Aβ-proteopathy and tauopathy in Alzheimer's disease remains largely undefined. Aβ plaques develop and propagate via the misfolding, self-assembly and spread of Aβ by the prion-like mechanism of seeded protein aggregation. Partially overlapping sets of risk factors and sequelae, including inflammation, genetic variations, and various environmental triggers have been linked to plaque development and idiopathic Alzheimer's disease, but no single factor has emerged as a requisite cause. The value of Aβ plaques per se as therapeutic targets is uncertain; although some plaques are sites of focal gliosis and inflammation, the complexity of inflammatory biology presents challenges to glia-directed intervention. Small, soluble, oligomeric assemblies of Aβ are enriched in the vicinity of plaques, and these probably contribute to the toxic impact of Aβ aggregation on the brain. Measures designed to reduce the production or seeded self-assembly of Aβ can impede the formation of Aβ plaques and oligomers, along with their accompanying abnormalities; given the apparent long timecourse of the emergence, maturation and proliferation of Aβ plaques in humans, such therapies are likely to be most effective when begun early in the pathogenic process, before significant damage has been done to the brain. Since their discovery in the late 19th century, Aβ plaques have, time and again, illuminated fundamental mechanisms driving neurodegeneration, and they should remain at the forefront of efforts to understand, and therefore treat, Alzheimer's disease.

Neurocutaneous disorders are a heterogeneous group of genetic disorders that include Sturge-Weber syndrome (SWS), which is characterized by congenital capillary-venous malformation manifesting as port-wine stain, leptomeningeal angiomatosis and ocular angiomas. Diagnosis is made when at least two of these three areas are involved. Abnormal vessels lead to stasis and congestion resulting in decreased regional perfusion and eventually cause hypoxic brain injury with neuronal loss and gliosis. Seizures are common neurological manifestation in SWS patients and many patients have intractable seizures, eventually leading to motor deficits or developmental and cognitive delays. Here we report a case of a 16-year-old boy who presented with typical port-wine stain and seizure disorder since childhood. Neuroimaging revealed evidence of cerebral vascular malformation ipsilateral to the cutaneous lesion. Seizure was controlled with antiepileptic drugs. Early diagnosis and prompt treatment may reduce the incidence of neurologic sequelae. Proper counselling is necessary to improve compliance.

Objective To investigate the neuroprotective effect of Benztropine on retinal ganglion cells(RGCs) death and optic nerve injury in rats model of non-arteritis anterior ischemic optic neuropathy (rNAION). Methods A total of 25 Sprague-Dawley rats were randomly divided into Benztropine treatment group (n=13) and PBS control group (n=12). The right eye was set as the experimental eye. rNAION model was established by using rose Bengal combined with laser photodynamic method. The rats in the Benztropine treatment group were received intraperitoneal injection with Benztropine 10 mg/kg (0.2 ml) daily for 3 weeks, while the rats in the PBS control group were received intraperitoneal injection with an equal volume of PBS. At 1, 3 and 7 days after modeling, the retinal and optic disc conditions of the rats were observed by direct ophthalmoscopy. Retrograde labeling, fluorescence microscopy and transmission electron microscopy were used to observe the survival of RGCs and the damage of the optic nerve myelin and axon at 4 weeks after modeling. The RGCs density and survival rate of the two groups were compared by One-Way Anova. Results At 1 and 3 days after modeling, the optic disc edema was observed in the rats of rNAION model group. At 7 days after modeling, the optic disc edema decreased and the boundary was blurred compared with 3 days after modeling.After 4 weeks, the RGCs density in the PBS group was 308±194/mm2 and the survival rate was 13.7%. The density of RGCs in the Benztropine group was 1173+868/mm2 and the survival rate was 47.6%. The differences of RGCs density and survival rate were significant between the two groups (F=7.552, 8.184; P=0.015, 0.012). Myelin disintegration, axon degeneration, onion-like body and gliosis were observed in the optic nerve sections of rNIAON in the PBS group, while the damage of axon and myelin structure in the Benztropine group was significantly less than that in the PBS group. Conclusions Benztropine group showed higher RGC survival rate, less damage of axon and myelin structure on rNAION model. This study explored the potential neuroprotective effect of Benztropine. Key words: Optic neuropathy, ischemic; Retinal ganglion cells; Disease models, animal

In mammalian retina, Muller cells are dominating macroglial cells and span the entire retina.These cells perform a variety of physiological roles to maitain the normal function of retina.However, Muller cells become'reactivity’in response to every pathological changes in the retina.Reactive Muller cells play an important role in retinal damage and repair.Reactive gliosis is a complex process that is considered to represent a cellular response to protect the retina from further damage and to promote its repair following pathological insult in the early stage of retina injury.Reactive Muller cells protect the tissue and preserve tissue function by releasing neurotrophic factors, and may contribute to retinal regeneration by generating neural progenitor.However, continued proliferation of Muller cells can also lead to cell dysfunction and damage of photoreceptors and neurons.What's more, Muller cell gliosis may result in the formation of glial scars, which can inhibit retinal remodeling and reprograming of the injured retina.A better understanding of the role and mechanism of Muller cells in retinopathy is essential for the efficient therapeutic strategies of retina diseases. Key words: Muller cell; Retinal diseases; Gliosis; Glial scars

Double inversion recovery in detection of perilesional gliosis in calcific cysticercosis.

The use of glucocorticoid agonists in treating acute attacks of multiple sclerosis is well established. Relaxin, a member of the insulin super family is a pleiotropic hormone capable of influencing multiple pathways which include the glucocorticoid receptor and relaxin family peptide receptors 1 and 2. In addition to the action of relaxin on the glucocorticoid receptor, activation of the relaxin receptors have additional anti-inflammatory and immuno-modulating effects. In the present study we investigated the effectiveness of relaxin in treating a murine model of MS, experimental allergic encephalomyelitis. Disease was induced and the mice were scored daily for clinical signs of disease (0=normal, 3=hind limb paralysis, 5=found dead). When a clinical score of 3 or higher was reached, relaxin was continuously infused for 8 days. Plasma for RT-PCR and spinal cords for histology were collected. The levels of CCR2, CCR5, CCR7, interleukins-6 and 17 were analyzed using quantitect primers and SYBR green based RT-PCR kits. Spinal cords were formalin fixed, paraffin embedded, sectioned and scored for myelin content, macrophage infiltration, neurofilaments, gliosis and markers of remyelination. The results of the study show that continuous infusion of relaxin significantly reduced the clinical signs of disease, decreased mRNA expression of pro-inflammatory cytokines and chemokine receptors. Histological staining and immune-histochemistry of the spinal cords showed that relaxin treatment lead to a decrease in lesion load and size and macrophage infiltration, preserved myelin and neurofilaments, reduced gliosis and promoted remyelination.

The reattachment rate, macular hole (MH) closure rate, visual acuity improvement and redetachment rate of MH retinal detachment (MHRD) of high myopia are not satisfactory owing to long axis oculi, posterior scleral staphyloma and macular atrophy. At present, minimally invasive vitrectomy surgery combined with the internal limiting membrane flap technique has become popular in the treatment of MHRD, as it can promote MH closure, and significantly improve the outcome of MHRD. However if this method can improve the postoperative visual function is still controversial. The advantage of this technique is that the loosened internal limiting membrane is applied to cover the MH surface to form a scaffold structure similar to the basement membrane. It can stimulate Muller cell gliosis more effectively, and promote tissue filling in the MH which results in MH closure. It can also promote retinal reattachment and reduce the likelihood of retinal redetachment. This technique is expected to be a standard surgical method for the treatment of MHRD of high myopia in the future. The inserted internal limiting membrane flap technique is relatively easy to perform, induces stable flaps by simple procedures, and can be an essential complement procedure of the inverted internal limiting membrane flap technique. In order to reduce the recurrence rate in the future, it is necessary to further define the indications of different surgical methods and the predictive effects of MH healing mode on the success rate and visual function recovery. Key words: Myopia, degenerative/complications; Retinal perforations/surgery; Retinal detachment/ surgery; Vitreoretinal surgery; Epiretinal membrane; Editorial

A demyelinating sickness is any ailment of the nervous system in which the myelin casing of neurons is injured. This harm weakens the transmission of signals in the pretentious nerves. Demyelinating diseases, like multiple sclerosis (MS) and Charcot-Marie-Tooth (CMT) disease, are categorized on the basis of the scratch of the myelin covering around neurons, because of swelling and gliosis in the central nervous system (CNS) and peripheral nervous system (PNS), respectively. In this current research, an amalgam approach of comparative modeling and molecular docking pursued by inhibitor recognition and structure modeling was used. Existing treatments mark anti-inflammatory ways to hinder or slow disease sequence. The recognition of a means to improve axon myelination would present innovative remedial approaches to restrain and probably turn around disease progression. A computational ligand-target docking method was applied to investigate structural composites of the Leucine Rich Repeat and Ig Domain Containing 1 (LINGO1) with three ligands to understand the structural foundation of this protein goal specificity. The following ten residues were conserved for all the three ligands interaction LEU133, ILE134, Pro135, LEU136, ILE155, ILE157, LEU159, ASP160, TYR161, and MET162 which are present in Leucine Rich Repeat 3 and 4 domains. Therefore, these three ligands can be utilized as the potential inhibitors to prevent various neurological disorders and the axonal neuropathies especially the CMT disease. Docking analysis showed that the two important drugs which are widely used have the potential to block the Rho-Rock pathways. Here, we report inhibitors which showed maximum binding affinity for the three most important axonal regeneration inhibitors. However, further studies are required to find the applications of these drugs. Key words: Demyelination, RTN4, CMT1A, spinal cord injury, ROCK inhibition, neurite growth inhibitors.

The neuroretinal injuries of diabetic retinopathy (DR) include retinal neuronal damage and reactive gliosis, both of which are induced by hyperglycemia and presented as early features of DR. They promote to develop mutually and accelerate the progression of DR. The molecular mechanisms study of neuronal damage mainly focuses on the alterations of extracellular environment and related signaling pathways, include inflammation, oxidative stress, endoplasmic reticulum stress, the formation of advanced glycation end products, glutamate toxicity and so on. These alterations mainly result in neuronal apoptosis and autophagy. The damaged neurons activate the glial cells with apparent changes in morphology, cell counts and the level of intracellular protein expression. In non-proliferative DR, glial cells are moderately hypertrophic and slightly increased in numbers. In proliferative DR, there is a significant rise in glial cell number with enhanced level of inflammatory factors and vascular active substances which lead a further neuronal damage. Signaling pathways of extracellular signal-regulated kinase 1/2, c-Fos and p38 mitogen-activated protein kinase are associated with their activation. Researches on the molecular mechanisms and signaling pathways of the DR will promote controlling the DR progression at the cellular level. Key words: Optic nerve injuries; Diabetic retinopathy/pathology; Apoptosis; Autophagy; Review

Negative control of immunofluorescence labels. Retinal sections from P30 mouse labeled with rabbit immunoglobulin G (Rbt IgG; A–C, D, F), mouse IgG (Mse IgG; E, F), and sheep IgG (G, H) to determine background fluorescence. Images of sections labeled with the nuclear stain, Hoechst merged with the images of green and red channels are shown in C and F. Panels A–C represent sections, which were labeled with IgG following the procedure used for tyramide amplification when using two antibodies for the same species. Images in D–F represent sections co-labeled with rabbit and mouse IgG. Images A–C are negative controls for Fig. 1 and Additional file 1: Figure S1. Images D–F are negative controls for sections labeled with GFAP, S100-β, Calbindin, Brn3a, Chx10, Sox9, and IBA1. Images G and H are negative control sections for NCAN-labeled slides. Magnification bar in A = 50 μm, for images A–H. (TIF 465 kb)

Objective To investigate the phenotypes and genetics of an early-onset familial Alzheimer′s disease (EO-FAD) family. Methods The clinical manifestations, brain MRI results and neuropathological findings of the proband and pedigree members of the EO-FAD family were evaluated. Autopsy was performed in the proband. Results Fifteen members of this family had a presenilin 1 (PSEN1) p. G378E mutation and nine of them had clinical manifestations or the MRI changes of EO-FAD. Neuropathological findings from autopsy of the proband disclosed moderate cortical atrophy throughout the brain, especially in frontal lobe and temporal lobe. Neuronal loss with gliosis was observed in the cortices of the frontal, temporal and occipital lobes, as well as in parahippocampal gyrus. Numerous senile plaques and neurofibrillary tangles were present in the cerebral cortex. The proband′s younger sister showed similar clinical presentations and MRI changes, and other members of this family demonstrated progressive memory loss. Conclusion A p. G378E mutation in the PSENl gene was identified in a Chinese EO-FAD pedigree. Key words: Alzheimer disease, familial; PSEN1 gene; Gene mutation

Background and Aim. Obesity is a metabolic disorder with an increasing incidence in Western countries and childhood. It is characterized by low-grade systemic inflammation and several comorbidities, including alterations of gastrointestinal (GI) functions, which impact negatively on patients’ quality of life. There is currently limited information on the morpho-functional features of the GI tract in obese subjects. Of note, the intestinal barrier function has been found to be altered in obese subjects, even before the occurrence of body weight increase [1]. In this light, the present study was carried out to assess, in a mouse model of diet-induced obesity, whether high fat diet (HFD) is associated with morphological alterations of the colonic mucosal barrier. Methods. C57BL/6 mice (n=5/group) were fed with standard diet (SD, 18% calories from fat) or HFD (60% calories from fat). After 8 weeks, body weight, and levels of blood cholesterol, triglycerides and glucose were evaluated. Malondialdehyde (MDA, colorimetric assay), IL-1β and IL-6 levels (ELISA assays) were examined in colonic tissues. Morphological features of colonic mucosal structures (lining epithelial cells, goblet cells, inflammatory infiltrates and enteric glia) were examined by histochemistry and immunohistochemistry. Results. HFD mice displayed significant differences at both molecular and histomorphological level, as compared with SD animals: increased body weight and blood metabolic indexes; increased MDA, IL-1β and IL-6 levels in colonic tissues; altered pattern of claudin-1 expression along with upregulation of transmembrane 16A protein and induced nitric oxide synthase in the enteric epithelium facing the lumen; increased proliferation rate of crypts; altered composition of goblet cell mucous; mucosal gliosis and infiltrates with mixed inflammatory cells. Conclusions. After 8 weeks, HFD intake led to significant alterations of systemic metabolic indexes, colonic tissue inflammation, and colonic mucosal barrier in obese mice, as compared with controls. Morphological studies can be useful to allow the characterization of histopathological patterns of colonic wall remodelling and inflammation underlying bowel motor dysfunctions associated with obesity.

Mitochondrial oxidative stress is an important pathologic factor in neurodegenerative diseases, including Alzheimer’s disease. Abnormal production of reactive oxygen species (ROS), resulting from mitochondrial dysfunction, leads to neuronal cell death. Ceria (CeO2) nanoparticles less than 5 nm are known to perform as powerful and recyclable ROS scavengers by exchanging between Ce3+ and Ce4+ oxidation states. Hence, targeting ceria nanoparticles specifically to mitochondria might be a promising therapeutic approach for neurodegenerative diseases. Here, we report the design and synthesis of triphenylphosphonium-conjugated ceria nanoparticles which localize to mitochondria of subicular cells due to their small hydrodynamic diameter (22 nm) and highly positive charge (+45 mV). The triphenylphosphonium-conjugated ceria nanoparticles diminish mitochondrial oxidative stress and suppress neuronal death in a 5XFAD transgenic Alzheimer’s disease mouse model after two months. The triphenylphosphonium-conjugated ceria nanoparticles alleviate reactive gliosis and morphological mitochondria damage observed in these mice. Altogether, our data indicate that the triphenylphosphonium-conjugated ceria nanoparticles are a potential therapeutic candidate for mitochondrial oxidative stress in Alzheimer’s disease.

Objective To investigate the neuroprotective effects of anterior thalamic nuclei(ANT)stimulation on hippocampal neurons in epileptic monkeys. Methods Eight male rhesus monkeys were randomly assigned to a model control group, a sham-stimulation group, and a stimulation group. A monkey model of temporal lobe epilepsy was induced by injection of kainic acid in the left hippocampus. The seizure frequency was compared in each group. At 6 months after modeling, immunohistochemical method was used to observe the pathological injury and fibrosis in hippocampal tissue. Western blot was used to quantitatively analyze the contents of heat shock protein-70(HSP-70), NeuN, and caspase-3 in hippocampal tissue. Results All animals that received the kainic acid injections had seizures. The total number of seizures in the stimulation group was 11.2±2.3 times, compared with 21.0±4.8 times in the sham-stimulation group, it decreased 42.8%(P 0.05). The content of NeuN in sham-stimulation group was significantly lower than that in the control group and the stimulation group(P<0.01, P<0.05). The content of Caspase-3 in sham-stimulation group was significantly higher than that in the control group and the stimulation group(P<0.01, P<0.05). Conclusions Long-term ANT stimulation may reduce the hippocampal injury and gliosis in temporal lobe epilepsy monkeys. This may be an important mechanism of ANT stimulation for the treatment of temporal lobe epilepsy. Key words: Epilepsy, temporal lobe; Anterior thalamic nuclei; Deep brain stimulation; Hippocampus; Rhesus monkeys

Objective To examine the expression of translocator protein (TSPO) in an intracerebral hemorrhage model in mice. Methods A intracerebral hemorrhage model in mice was induced by using autologous blood injection. The 28-point neurological deficit scale was used to evaluate neurological deficits of different amount of bleeding in the two group of mice (the mean amount of bleeding was 15 μl and 25 μl respectively) at day 1 after intracerebral hemorrhage, and Western blot was used to detect the expression levels of TSPO in the sham operation group, the amount of bleeding 15 μl group, and the amount of bleeding 25 μl group. Western blot and immunofluorescence staining were used to detect the TSPO expression at 12 h, day 1, 3, and 5 after modeling in mice in the amount of bleeding 25 μl group. Results The results of the 28-point neurological deficit scale showed that the neurological defect scores of the 2 groups of intracerebral hemorrhage model mice were significantly higher than the sham operation group (all P 0.05). The TSPO expression level increased gradually at day 1, 3, and 5 after modeling, and it was higher than the sham operation group (all P<0.05). Immunofluorescence staining results showed that the TSPO expression was not obvious at 12 h after modeling, while it increased gradually at day 1, 3, and 5 after modeling, and they mostly expressed in microglia and astrocytes of the perihematomal brain tissue. Conclusions The TSPO expression increases in perihematomal brain tissue after intracerebral hemorrhage in mice. Its expression level is associated with the time after bleeding and bleeding volume, suggesting that it may be associated with the secondary inflammatory response and injury after intracerebral hemorrhage. Key words: Cerebral hemorrhage; Translocator protein; Gliosis; Mice

Digital images were used in applications such as astronomy, medicine, physics and biology, to record and analyze results from experiments Due to the features of the imaging system, the recorded images can be degraded by blurring and noise. Image deconvolution, or image deblurring, is the process of reconstructing or estimating the true image from the degraded one [1]. In order to optimize morphometrical analysis of Glial Fibrillary Acidic protein (GFAp)-immunoreactive astrocyte of the whole rat entorhinal cortex of both trimethyltin hydrochloride- and saline treated rats, large images of it (about 30 000 x 20 000 pixels) were digitized by a microscope with a X – Y motorized computer-managed stage and an autofocusing system, using an objective 40x, a digital camera 2560x1920 RGB. Moreover it has been optimized a procedure of deconvolution and segmentation under the NIH ImageJ system. Such large images were first deblurred, by Modified Residual Norm Steepest Descent (MRNSD) and Wiener Filter Preconditioned Landweber (WPL) algoritms, and segmented, then analyzed, to measure the % of the area (in µm2) occupied by GFAp-immunoreactive cell bodies and processes, and classical morphometrical parameters. Statistical analysis was performed to describe obtained data and to point out differences between segmented only versus deblurred-segmented images. Our results can be summarized as follows. 1. Large images can be an useful tool to identify precisely the distribution of reactive astrocytes in the rat entorhinal cortex. 2. Deconvolution avoid an overestimation of the area of immunoreative astrocytes of about 10-15%. Segmentation allow a measurement with improved accuracy, precision and uncertainty. 3. This approach is time consuming and requires a multi-core hardware with a large amount of available RAM.

The accidental ingestion of Karwinskia humboldtiana (Kh) fruit in humans and animals causes chronic or acute intoxication. Acute poisoning induces respiratory failure that progresses rapidly to death. Studies in animals intoxicated with Kh describe lesions in cerebral cortex, cerebellum, spinal cord, hippocampus and caudate nucleus. Kh intoxication in Wistar rats models the sub-lethal clinical phase observed in humans. Considering these reports, the present study analyzed the histopathological alterations within the striatum following experimental Kh intoxication. Twenty Wistar rats were divided into three groups (n =5) and were intoxicated with Kh fruit. A control group (n =5) was included. Animals were euthanized at several time points (48, 58 and 170 days post-intoxication). The brain was collected, divided and processed for conventional histology or electron microscopy. Sections were stained with hematoxylin and eosin, cresyl violet, Klüver-Barrera, and toluidine blue. Immunolabeling was performed for glial cells in the striatum, and the samples were analyzed with light microscopy. Morphometric and statistical analyses were performed. In control group, neurons, axon bundles and neuropil had a normal appearance. At 48 days, hyperchromic neurons with apparent decreased size were observed interspersed among the normal neurons. At 58 days, we observed an increased number of hyperchromic neurons and disorganization of the myelin sheath and neuropil. At 170 days, these alterations persisted in the paralysis group. In treated groups, we observed signs of gliosis and increased axonal diameters. This study is the first report that describes the histopathological alterations within the striatum caused by chronic intoxication with Kh fruit in the Wistar rat.

To observe the pathological changes in rabbits with spinal cord injury induced by decompression sickness (DCS), and to investigate the role of tumor necrosis factor-alpha (TNF-α) in spinal cord injury induced by DCS. Rabbits were randomly divided into normal control group, DCS group, and safe decompression group. The rabbit model of DCS was established. Light microscopy, real-time PCR, and immunohistochemical method were used to observe the pathomorphological changes in the thoracolumbar spinal cord and the mRNA and protein expression of TNF-α, respectively. The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) was used to observe the apoptosis in the spinal cord. In the DCS group, cavities formed in the white matter of spinal cord and gliosis occurred around necrotic areas. Moreover, the mRNA and protein expression of TNF-α was significantly higher in the DCS group than in the normal control group and the safe decompression group (P<0.01). The results of TUNEL showed that the number of positive apoptotic cells was significantly larger in the DCS group than in the normal control group and the safe decompression group (P<0.05). Apoptosis plays an important role in spinal cord injury induced by DCS. In the early stage of DCS, the massive release of TNF-α initiates apoptosis and contributes to the pathological changes in spinal cord injury induced by DCS.