Chondroitinase ABC combined with Schwann cell transplantation enhances restoration of neural connection and functional recovery following acute and chronic spinal cord injury

Schwann cell transplantation is considered one of the most promising cell-based therapy to repair injured spinal cord due to its unique growth-promoting and myelin-forming properties.A the Food and Drug Administration-approved Phase I clinical trial has been conducted to evaluate the safety of transplanted human autologous Schwann cells to treat patients with spinal cord injury.A major challenge for Schwann cell transplantation is that grafted Schwann cells are confined within the lesion cavity,and they do not migrate into the host environment due to the inhibitory barrier formed by injury-induced glial scar,thus limiting axonal reentry into the host spinal cord.Here we introduce a combinatorial strategy by suppressing the inhibitory extracellular environment with injection of lentivirus-mediated transfection of chondroitinase ABC gene at the rostral and caudal borders of the lesion site and simultaneously leveraging the repair capacity of transplanted Schwann cells in adult rats following a mid-thoracic contusive spinal cord injury.We report that when the glial scar was degraded by chondroitinase ABC at the rostral and caudal lesion borders,Schwann cells migrated for considerable distances in both rostral and caudal directions.Such Schwann cell migration led to enhanced axonal regrowth,including the serotonergic and dopaminergic axons originating from supraspinal regions,and promoted recovery of locomotor and urinary bladder functions.Importantly,the Schwann cell survival and axonal regrowth persisted up to 6 months after the injury,even when treatment was delayed for 3 months to mimic chronic spinal cord injury.These findings collectively show promising evidence for a combinatorial strategy with chondroitinase ABC and Schwann cells in promoting remodeling and recovery of function following spinal cord injury.

An expert consensus on the evaluation and treatment of acute thoracolumbar spine and spinal cord injury in China

This is an expert consensus on the evaluation and treatment of thoracolumbar spinal injury, estab- lished from February 2009 to July 2010. The expert consensus consists mainly of six parts with a total of 54 recommendations including the overview （one item）; pre-hospital care （one item）; evaluation and diagnosis （13 items）; treatment （23 items）; prevention and treatment of major com- plications （12 items）; and rehabilitation （four items）. This is the first time that Chinese experts have published a consensus on spine and spinal cord injury. The expert consensus was established based on Delphi methods, literature analysis, and clinical experiences. Each recommendation is supported by and was interpreted using multi-level evidences. The level of agreement with the rec- ommendation among the panel members was assessed as either low, moderate, or strong. Each panel member was asked to indicate his or her level of agreement on a 5-point scale, with ＂1＂ cor- respondJng to neutrality and ＂5＂ representJng maxJmum agreement. Scores were aggregated across the panel members and an arithmetic mean was calculated. This mean score was then translated into low, moderate, or strong. After all of the votes were collected and calculated, the results showed no low-level recommendations, 10 moderate-level recommendations, and 44 strong-level recom- mendations. An expert consensus was reached and was recognized by Chinese spine surgeons. Wide-scale adoption of these recommendations is urgent in the management of acute thora- columbar spine and spinal cord injury in a broader attempt to create a standard evaluation and treatment strategy for acute thoracolumbar spine and spinal cord injury in China.

Anesthetic considerations for patients with acute cervical spinal cord injury

Anesthesiologists work to prevent or minimize secondary injury of the nervous system and improve the outcome of medical procedures.To this end,anesthesiologists must have a thorough understanding of pathophysiology and optimize their skills and equipment to make an anesthesia plan.Anesthesiologists should conduct careful physical examinations of patients and consider neuroprotection at preoperative interviews,consider cervical spinal cord movement and compression during airway management,and suggest awake fiberoptic bronchoscope intubation for stable patients and direct laryngoscopy with manual in-line immobilization in emergency situations.During induction,anesthesiologists should avoid hypotension and depolarizing muscle relaxants.Mean artery pressure should be maintained within 85–90 mmHg（1 mmHg = 0.133 kPa; vasoactive drug selection and fluid management）.Normal arterial carbon dioxide pressure and normal blood glucose levels should be maintained.Intraoperative neurophysiological monitoring is a useful option.Anesthesiologists should be attentive to postoperative respiratory insufficiency（carefully considering postoperative extubation）,thrombus,and infection.In conclusion,anesthesiologists should carefully plan the treatment of patients with acute cervical spinal cord injuries to protect the nervous system and improve patient outcome.

Effects of decompression joint Governor Vessel electro-acupuncture on rats with acute upper cervical spinal cord injury

Decompression is the major therapeutic strategy for acute spinal cord injury,but there is some debate about the time window for decompression following spinal cord injury.An important goal and challenge in the treatment of spinal cord injury is inhibiting or reversing secondary injury.Governor Vessel electroacupuncture can improve symptoms of spinal cord injury by inhibiting cell apoptosis and improving the microenvironment of the injured spinal cord.In this study,Governor Vessel electroacupuncture combined with decompression at different time points was used to treat acute spinal cord injury.The rat models were established by inserting a balloon catheter into the atlanto-occipital space.The upper cervical spinal cord was compressed for 12 or 48 hours prior to decompression.Electroacupuncture was conducted at the acupoints Dazhui（GV14） and Baihui（GV 20）（2 Hz,15 minutes） once a day for 14 consecutive days.Compared with decompression alone,hind limb motor function recovery was superior after decompression for 12 and 48 hours combined with electroacupuncture.However,the recovery of motor function was not significantly different at 14 days after treatment in rats receiving decompression for 12 hours.Platelet-activating factor levels and caspase-9 protein expression were significantly reduced in rats receiving electroacupuncture compared with decompression alone.These findings indicate that compared with decompression alone,Governor Vessel electroacupuncture combined with delayed decompression（48 hours） is more effective in the treatment of upper cervical spinal cord injury.Governor Vessel electroacupuncture combined with early decompression（12 hours） can accelerate the recovery of nerve movement in rats with upper cervical spinal cord injury.Nevertheless,further studies are necessary to confirm whether it is possible to obtain additional benefit compared with early decompression alone.

Future directions for using estrogen receptor agonists in the treatment of acute and chronic spinal cord injury

All synthetic and natural estrogen receptor agonists, in- cluding the most potent physiological molecule estrogen or estradiol （E2）, work typically via activation of nuclear estrogen receptor alpha （ERα） and estrogen receptor beta （ERβ）. Both ERα and ERβ modulate the expression of a variety of genes in the cells. Neurons and glial cells express ERa and ERβ. Many studies so far from our and other laboratories have firmly established the mode of actions that ERα and ERβ agonists are very promising anti-inflammatory and neuroprotective agents in the treatment of neurodegenera- rive diseases and injuries including spinal cord injury （SCI） （Chakrabarti et al., 2014a）.

Provision of nutrients after acute spinal cord injury: the implications of feast and famine

Traumatic spinal cord injury（SCI）often leaves patients with devastating neurological deficits.The traumatic event–or primary injury–can be due to mechanisms such as compression,distraction,shear,laceration or（rarely）even transection.Thereafter SCI patients are vulnerable to progressive,delayed damage as a result of secondary insults and secondary injury.Secondary insults such as hypoxia and hypotension occur at the level of the organism from a myriad of causes.

Effect of FTY720 on RhoA expression after acute spinal cord injury in rats

Objective To investigate the effect of fingolimod (FTY720)on RhoA expression after spinal cord injury (SCI)in rats,and explore the possible mechanism of FTY720in the treatment of SCI.Methods A rat model of acute SCI was established with a

Collagen scaffold combined with human umbilical cord-mesenchymal stem cells transplantation for acute complete spinal cord injury

Currently, there is no effective strategy to promote functional recovery after a spinal cord injury. Collagen scaffolds can not only provide support and guidance for axonal regeneration, but can also serve as a bridge for nerve regeneration at the injury site. They can additionally be used as carriers to retain mesenchymal stem cells at the injury site to enhance their effectiveness. Hence, we hypothesized that transplanting human umbilical cord-mesenchymal stem cells on collagen scaffolds would enhance healing following acute complete spinal cord injury. Here, we test this hypothesis through animal studies and a phase I clinical trial.(1) Animal experiments: Models of completely transected spinal cord injury were established in rats and canines by microsurgery. Mesenchymal stem cells derived from neonatal umbilical cord tissue were adsorbed onto collagen scaffolds and surgically implanted at the injury site in rats and canines;the animals were observed after 1 week–6 months. The transplantation resulted in increased motor scores, enhanced amplitude and shortened latency of the motor evoked potential, and reduced injury area as measured by magnetic resonance imaging.(2) Phase I clinical trial: Forty patients with acute complete cervical injuries were enrolled at the Characteristic Medical Center of Chinese People's Armed Police Force and divided into two groups. The treatment group(n = 20) received collagen scaffolds loaded with mesenchymal stem cells derived from neonatal umbilical cordtissues;the control group(n = 20) did not receive the stem-cell loaded collagen implant. All patients were followed for 12 months. In the treatment group, the American Spinal Injury Association scores and activities of daily life scores were increased, bowel and urinary functions were recovered, and residual urine volume was reduced compared with the pre-treatment baseline. Furthermore, magnetic resonance imaging showed that new nerve fiber connections were formed, and diffusion tensor imaging showed that electrophysiological activity was recovered after the treatment. No serious complication was observed during follow-up. In contrast, the neurological functions of the patients in the control group were not improved over the follow-up period. The above data preliminarily demonstrate that the transplantation of human umbilical cord-mesenchymal stem cells on a collagen scaffold can promote the recovery of neurological function after acute spinal cord injury. In the future, these results need to be confirmed in a multicenter, randomized controlled clinical trial with a larger sample size. The clinical trial was approved by the Ethics Committee of the Characteristic Medical Center of Chinese People's Armed Police Force on February 3, 2016(approval No. PJHEC-2016-A8). All animal experiments were approved by the Ethics Committee of the Characteristic Medical Center of Chinese People's Armed Police Force on May 20, 2015(approval No. PJHEC-2015-D5).

Neuroprotective effects of the immunodepressant FTY720 on caspase-3 expression and neural apoptosis in a rat model of acute spinal cord injury

BACKGROUND：Studies on the immunodepressant FTY720 have primarily focused on organ transplantation and autoimmune disease therapy.However,the effects on caspase-3 expression and neural apoptosis following acute spinal cord injury remain uncertain.OBJECTIVE：To elucidate the underlying mechanism of the immunodepressant FTY720 to alleviate spinal cord injury by inhibiting expression of caspase-3 and neural apoptosis.DESIGN,TIME AND SETTING：A randomized,controlled,animal experiment was performed at Central Laboratory of the Second Affiliated Hospital of Dalian Medical University from April to July 2009.MATERIALS：FTY720 was provided by Wuhan Yuancheng Technology Developing,China.METHODS：A total of 120 Sprague Dawley rats were randomly assigned to sham-surgery,model,and FTY720 groups.Spinal cord injury at the T9-10 segment was induced in model groups using the free-fall method.Following establishment of spinal cord injury at the T9-10 segment in the FTY720 group,rats were treated with an intragastric injection of 0.3 mL saline-diluted FTY720 （3 mg/kg）.MAIN OUTCOME MEASURES：At 6,12,24,48,and 72 hours following spinal cord injury,caspase-3 expression was detected using streptavidin-peroxidase immunohistochemistry,and neural apoptosis was detected using the TUNEL method.RESULTS：Positive caspase-3 expression and neural apoptosis was not observed in the sham-surgery group at the various time points.The number of apoptotic cells increased with time after acute spinal cord injury,peaked at 24 hours following injury,and then gradually reduced.However,neural apoptosis remained at a high level.Caspase-3 expression positively correlated with neural apoptosis （r= 0.864,P〈 0.05）.Caspase-3 expression and neural apoptosis significantly decreased following FTY720 therapy （P〈 0.05）.CONCLUSION：FTY720 significantly reduced caspase-3 expression and neural apoptosis in a rat model of acute spinal cord injury.

Hydrogen-rich saline injection into the subarachnoid cavity within 2 weeks promotes recovery after acute spinal cord injury

Hydrogen can relieve tissue-damaging oxidative stress, inflammation and apoptosis. Injection of hydrogen-rich saline is an effective method for transporting molecular hydrogen. We hypothesized that hydrogen-rich saline would promote the repair of spinal cord injury induced by Allen＇s method in rats. At 0.5, 1, 2, 4, 8, 12 and 24 hours after injury, then once daily for 2 weeks, 0.25 mL/kg hydrogen-rich saline was infused into the subarachnoid space through a catheter. Results at 24 hours, 48 hours, 1 week and 2 weeks after injury showed that hydrogen-rich saline markedly reduced cell death, inflammatory cell infiltration, serum malondialdehyde content, and caspa se-3 immunoreactivity, elevated serum superoxide dismutase activity and calcitonin gene-related peptide immunoreactivity, and improved motor function in the hindlimb. The present study confirms that hydrogen-rich saline injected within 2 weeks of injury effectively contributes to the repair of spinal cord injury in the acute stage.

Effects of low dose Glibenclamide on secondary damage after acute spinal cord injury in rats

Objective To investigate the effects of Glibenclamide on reduction of secondary damage after acute spinal cord injury in rats.Methods Ninety rats were randomly divided into control group(laminectomy alone),spinal cord injury group(injury group),and treatment group(treated

Factors related to improved American Spinal Injury Association grade of acute traumatic spinal cord injury

BACKGROUND Acute traumatic spinal cord injury(ATSCI)usually results in disability,yet data on contemporary national trends of ATSCI incidence are limited.AIM To provide a systematic and basic theoretical basis for improving the treatment of acute spinal cord injury.METHODS Data from the Peking University Third Hospital Inpatient Sample databases were analyzed.A total of 304 patients with ATSCI were included from 2012 to 2017.The epidemiological data,treatment,complications and clinical outcomes of these patients were reviewed.RESULTS Of the 304 patients,257(84.5%)were male,and 75%of the patients were 55 years old or younger.135 patients had improved follow-up American Spinal Injury Association(ASIA)grades(44.4%).Only 14 patients with ASIA grade A improved.A statistically significant difference in prognosis between patients who underwent surgery within 72 h and those who underwent surgery after 72 h was observed(P<0.05).Surgery within 72 h resulted in better prognosis.The Steroid group and the Non-Steroid group showed a significant difference in outcome among patients with ASIA grades A and B(P<0.05).Patients with pneumonia had a poorer prognosis than patients without pneumonia(P<0.05).Surgery within 72 h resulted in better prognosis.CONCLUSION This study found that there was no significant difference in hospitalization time and prognosis between the Steroid group and the Non-Steroid group,but the patients with severe spinal cord injury(ASIA grades A and B)who underwent surgery combined with steroid therapy had a better prognosis than those who underwent surgery alone.The disastrous consequences of ATSCI and lack of consensus on the management strategy are obvious.Further improvements in treatment planns are needed in order to obtain more reliable functional outcomes.

Methylprednisolone inhibits Nogo-A protein expression after acute spinal cord injury

Oligodendrocyte-produced Nogo-A has been shown to inhibit axonal regeneration. Methylprednisolone plays an effective role in treating spinal cord injury, but the effect of methylprednisolone on Nogo-A in the injured spinal cord remains unknown. The present study established a rat model of acute spinal cord injury by the weight-drop method. Results showed that after injury, the motor behavior ability of rats was reduced and necrotic injury appeared in spinal cord tissues, which was accompanied by increased Nogo-A expression in these tissues. After intravenous injection of high-dose methylprednisolone, although the pathology of spinal cord tissue remained unchanged, Nogo-A expression was reduced, but the level was still higher than normal. These findings implicate that methylprednisolone could inhibit Nogo-A expression, which could be a mechanism by which early high dose methylprednisolone infusion helps preserve spinal cord function after spinal cord injury.

Injury potentials associated with severity of acute spinal cord injury in an experimental rat model

To investigate characteristics of injury potentials after different degrees of spinal cord injury in rats the present study established models of spinal cord contusion with severe, moderate, and mild degrees of injury. Injury potential was measured in vivo using a direct current voltage amplification system. Results revealed that in the first 4 hours after acute spinal cord injury, initial amplitude of injury potential was greatest after severe injury, followed by moderate and mild injuries. Amplitude of injury potential decreased gradually with injury time, and the recession curve was logarithmic. Under the same degree of injuries, amplitude of rostral injury potential was generally less than caudal injury potential. Results suggested that injury potential reflected injury severity, because large initial amplitude of injury potential during the early injury stage implied severe injury.

Management of acute spinal cord injury:A summary of the evidence pertaining to the acute management,operative and non-operative management

Acute traumatic spinal cord injury is often a lifechanging and devastating event with considerable mortality and morbidity.Over half a million people suffer from traumatic spinal cord injury annually with the majority resulting from road traffic accidents or falls.The Individual,societal and economic costs are enormous.Initial recognition and treatment of acute traumatic spinal cord injury are crucial to limit secondary injury to the spinal cord and to provide patients with the best chance of some functional recovery.This article is an overview of the management of the acute traumatic spinal cord injury patient presenting to the emergency department.We review the initial assessment,criteria for imaging and clearing the spine,and evaluate the literature to determine the optimum timing of surgery and the role of non-surgical treatment in patients presenting with acute spinal cord injury.

Evidence-based treatment for acute spinal cord injury

OBJECTIVE： To formulate an evidence-based treatment for one patient with acute spinal cord injury and summarize evidence for evaluating acute spinal cord injury treatment. METHODS： Studies related to the treatment for acute spinal cord injury were identified via a search of National Guideline Clearinghouse （NGC, 2000 11）, the Cochrane Library （Issue 1,2011）, TRIP Database （2000 11）, and PubMed （1966-2011）. Treatment strategies were formulated according to three basic principles： best evidence, doctor＇s professional experience, and wishes of the patient. RESULTS： A total of 34 articles were selected, including 1 NGC guideline, 22 systematic reviews, and 11 randomized controlled trials. Based on our review, we arrived at the following recommendations： no clinical evidence exists definitively to recommend the use of any of neuroprotective pharmaceuticals; surgery should be undertaken early; mechanical compression devices and low-molecular weight heparin should be employed to prevent thrombosis; respiratory muscle training is beneficial for pulmonary function and quality of life; and functional electrical stimulation and acupuncture can promote functional recovery. The patient accordingly underwent surgery 6 hours after trauma without receiving any neuroprotective pharmaceuticals; low-molecular weight heparin and intermittent pneumatic compression were applied to prevent thrombosis. He also underwent respiratory muscle training daily for 8 weeks and received functional electrical stimulation for 15 minutes and acupuncture for 30 minutes every day. After follow-up for 3 months, the above therapeutic regimen was confirmed efficacious for acute spinal cord injury. CONCLUSION： Evidence-based medicine provides an individualized treatment protocol for acute spinal cord injury, which can significantly improve the therapeutic effect and prognosis.

Effect of neurotrophin-3 on SOD and MDA in rats after acute spinal cord injury

Objective:To investigate the effect of neurotrophin-3 on the expressions of SOD and MDA in the injured spinal cord of rats. Methods: Totally 105 SD rats were randomly divided into 3 groups (n = 35): sham group, control group and experimental group. Animal model of acute spinal cord was inflicted with Allen's method by a thin plastic tube situated in subarachnoid space below the injury level for perfusion. Rats in experimental group received 20μl NT-3 (200 ng) from the tube at 0, 4. 8. 12. 24 h and 3. 7 d after injury, and those in control group got the equal volume of normal saline at the same time points. The animals in sham group only received opening vertebral plate and putting tube in subarachnoid space. The rats were sacrificed at 4, 8. 12. 24 h, and 3. 7, 14 d postinjury (n = 5). And the levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in blood were observed with colorimetric method. Results: The serum level of SOD reduced obviously and the level of MDA raised obviously in rats after the injury, and the activity of SOD reached the lowest on day 3 and the concentration of MDA reached peak at the 7 d. In the experimental group, the SOD level was obviously higher (P<0. 01). and MDA level was lower than the control (P<0. 01). Conclusion:NT-3 can mitigate secondary injury of spinal cord in vivo. One of mechanisms is that inhibits abnormal expression of MDA and elevates the activity of SOD. thus the injury of free radical and lipid peroxidation is attenuated.

Time representation of mitochondrial morphology and function after acute spinal cord injury

Changes in mitochondrial morphology and function play an important role in secondary damage after acute spinal cord injury. We recorded the time representation of mitochondrial morphology and function in rats with acute spinal cord injury. Results showed that mitochondria had an irregular shape, and increased in size. Mitochondrial cristae were disordered and mitochondrial membrane rupture was visible at 2–24 hours after injury. Fusion protein mitofusin 1 expression gradually increased, peaked at 8 hours after injury, and then decreased to its lowest level at 24 hours. Expression of dynamin-related protein 1, amitochondrial fission protein, showed the opposite kinetics. At 2–24 hours after acute spinal cord injury, malondialdehyde content, cytochrome c levels and caspase-3 expression were increased, but glutathione content, adenosine triphosphate content, Na＋-K＋-ATPase activity and mitochondrial membrane potential were gradually reduced. Furthermore, mitochondrial morphology altered during the acute stage of spinal cord injury. Fusion was important within the first 8 hours, but fission played a key role at 24 hours. Oxidative stress was inhibited, biological productivity was diminished, and mitochondrial membrane potential and permeability were reduced in the acute stage of injury. In summary, mitochondrial apoptosis is activated when the time of spinal cord injury is prolonged.

Neuroprotective effects of a ketogenic diet in combination with exogenous ketone salts following acute spinal cord injury

We have previously shown that induction of ketosis by ketogenic diet(KD)conveyed neuroprotection following spinal cord injury in rodent models,however,clinical translation may be limited by the slow raise of ketone levels when applying KD in the acute post-injury period.Thus we investigated the use of exogenous ketone supplementation(ketone sodium,KS)combined with ketogenic diet as a means rapidly inducing a metabolic state of ketosis following spinal cord injury in adult rats.In uninjured rats,ketone levels increased more rapidly than those in rats with KD alone and peaked at higher levels than we previously demonstrated for the KD in models of spinal cord injury.However,ketone levels in KD+KS treated rats with SCI did not exceed the previously observed levels in rats treated with KD alone.We still demonstrated neuroprotective effects of KD+KS treatment that extend our previous neuroprotective observations with KD only.The results showed increased neuronal and axonal sparing in the dorsal corticospinal tract.Also,better performance of forelimb motor abilities were observed on the Montoya staircase(for testing food pellets reaching)at 4 and 6 weeks post-injury and rearing in a cylinder(for testing forelimb usage)at 6 and 8 weeks post-injury.Taken together,the findings of this study add to the growing body of work demonstrating the potential benefits of inducing ketosis following neurotrauma.Ketone salt combined with a ketogenic diet gavage in rats with acute spinal cord injury can rapidly increase ketone body levels in the blood and promote motor function recovery.This study was approved by the Animal Care Committee of the University of British Columbia(protocol No.A14-350)on August 31,2015.

Effect of interleukin-2 on neurogliocyte and neuron apoptosis in rat models of acute spinal cord injury

BACKGROUND： lnterleukin-2 （IL-2） may influence the growth and survival of nerve cells following spinal cord injury and resuscitate the proliferation and maturation of oligodendrocytes. OBJECTIVE： To observe the effect of IL-2 on neuronal apoptosis of neurogliocytes at different times following acute spinal cord injury in rats. DESIGN, TIME AND SETTING： A randomized grouping trial based on cellular morphology was performed at the Institute of Traumatic Orthopedics of Shandong Province between October 2004 and January 2006. MATERIALS： A total of 72 adult, male, Sprague Dawley rats were included in this study and were divided into a control group and an IL-2 group. The Bcl-2 monoclonal antibody and TUNEL kit were purchased from Wunan Boster Biological Technology Corporation. METHODS： Spinal cord injury was induced in all the rats by dropping a weight from a height of 25 cm onto the exposed spinal cord at vertebral levels T7-11, thus producing a mild lesion. Immediately following the modeling, the rats were injected with daily IL-2 （10 uL） intramuscularly （the IL-2 group）. Other rats received an injection of physiological saline 0.5 mL/d （the control group）. MAIN OUTCOME MEASURES： Bcl-2 immunohistochemistry was applied to detect the Bcl-protein and positive cell expression. The TUNEL method was used to count the number of apoptotic cells. RESULTS： The expression level of Bcl-2 proteins increased significantly in spinal cord tissues during the first day after acute spinal cord injury, reaching a peak on days 3 and days 8 in the control and IL-2 groups, respectively. They were more prevalent in neurogliocytes than in neurocytes, and then began to decrease on day 14. From then until day 21, less expression was detected （P 〈 0.05）. In the control group, many apoptotic cells existed after 24 hours, and most of them were gliocytes; apoptotic cells reached a peak after 3-8 days. They then decreased gradually until day 21, when a small number of cells were still available. In the IL-2 group, the number of positive cells was significantly lower than in the control group （P 〈 0.05）. CONCLUSION： The expression of Bcl-2 and the number of apoptotic cells in neurogliocytes undergo similar changes with time after acute spinal cord injury. IL-2 may upregulate the expression of Bcl-2 proteins and decrease cell apoptosis in spinal cord tissue.