大鼠脊髓损伤后巢蛋白表达

目的探讨成年大鼠脊髓损伤后损伤区局部巢蛋白（nestin）的表达及意义。方法应用Allen＇s法建立大鼠脊髓拟伤模型，行为学评分采用BBB评分（Basso，Beattie＆Bresnahan locomotor rating scale，BBB scale），观察局部病理组织学改变及用免疫荧光组织化学方法检测局部脊髓在不同时段nestin的阳性表达变化。结果伤后1w BBB评分最低，随后增加，到4w以后达到最高并进入平台期。常规病理学检查显示拟伤模型类似于临床常见的脊髓损伤。损伤后1W，可见损伤区附近nestin表达升高，2W达高峰，4W后nestin表达明显下调。结论脊髓损伤可诱导损伤区周围短暂的nestin阳性表达，后者可能存在脊髓损伤后的再生与修复中起重要作用。     

Electrical stimulation modulates injury potentials in rats after spinal cord injury

An injury potential is the direct current potential difference between the site of spinal cord injury and the healthy nerves.Its initial amplitude is a significant indicator of the severity of spinal cord injury,and many cations,such as sodium and calcium,account for the major portion of injury potentials.This injury potential,as well as injury current,can be modulated by direct current field stimulation;however,the appropriate parameters of the electrical field are hard to define.In this paper,injury potential is used as a parameter to adjust the intensity of electrical stimulation.Injury potential could be modulated to slightly above 0 mV(as the anode-centered group) by placing the anodes at the site of the injured spinal cord and the cathodes at the rostral and caudal sections,or around -70 mV,which is resting membrane potential(as the cathode-centered group) by reversing the polarity of electrodes in the anode-centered group.In addition,rats receiving no electrical stimulation were used as the control group.Results showed that the absolute value of the injury potentials acquired after 30 minutes of electrical stimulation was higher than the control group rats and much lower than the initial absolute value,whether the anodes or the cathodes were placed at the site of injury.This phenomenon illustrates that by changing the polarity of the electrical field,electrical stimulation can effectively modulate the injury potentials in rats after spinal cord injury.This is also beneficial for the spontaneous repair of the cell membrane and the reduction of cation influx.     

Expression of Nemo-like kinase after spinal cord injury in rats

Wnt can induce signal transduction via the canonical pathway, which was involved in many processes in the nervous system. Nemo-like kinase (NLK) acts as a negative regulator of β-catenin/T-cell factor/lymphoid enhancer factor (LEF) and functions downstream of transforming growth factor β-activated kinase-1 in the Wnt signaling pathway. In this study, we performed a spinal cord injury (SCI) test in adult Sprague–Dawley rats and investigated the dynamic changes and role of NLK expression in the spinal cord. Western blot analysis revealed that NLK expression was low in normal spinal cord. It then increased markedly, peaked at 3 days, and declined to basal levels from 5 days after injury. Immunohistochemistry confirmed that NLK immunoactivity was expressed at low levels in gray and white matter under normal conditions and increased prominently in gray matter after the SCI test. Double immunofluorescent staining for NLK, caspase-3, β-catenin, and NeuN (neuronal nuclei) revealed that NLK and β-catenin were markedly increased and colocalized in apoptotic neurons. Coimmunoprecipitation data demonstrated that overexpression of NLK protein reduced β-catenin binding to LEF-1. Our results suggested that NLK was associated with neuronal apoptosis through attenuating the Wnt/β-catenin signaling pathway after SCIs.     

Gastric dysreflexia after acute experimental spinal cord injury in rats

Abstract  Gastric reflexes are mediated mainly by vago-vagal reflex circuits in the caudal medulla. Despite the fact that brainstem vago-vagal circuitry remains intact after spinal cord injury (SCI), patients with SCI at the cervical level most often present gastric stasis with an increased risk of reflux and aspiration of gastric contents. Using a miniature strain gauge sutured to the gastric surface; we tested gastric motility and reflexive gastric relaxation following oesophageal distension (oesophageal-gastric relaxation reflex) in animals 3 days after a severe spinal contusion at either the third or ninth thoracic spinal segment (acute T3- or T9 SCI, respectively). Both basal gastric motility and the oesophageal-gastric relaxation reflex were significantly diminished in animals with T3 SCI. Conversely, both basal gastric motility and the oesophageal-gastric relaxation reflex were not significantly reduced in T9 SCI animals compared to controls. The reduced gastric motility and oesophageal-gastric reflex in T3 SCI rats was not ameliorated by celiac sympathectomy. Our results show that gastric stasis following acute SCI is independent of altered spinal sympathetic input to the stomach caudal to the lesion. Our data suggest that SCI may alter the sensitivity of vagal reflex function, perhaps by interrupting ascending spinosolitary input to brainstem vagal nuclei.     

Spontaneous long-term remyelination after traumatic spinal cord injury in rats

The capability of the central nervous system to remyelinate axons after a lesion has been well documented, even though it had been described as an abortive and incomplete process. At present there are no long- term morphometric studies to assess the spinal cord (SC) remyelinative capability. With the purpose to understand this phenomenon better, the SC of seven lesionless rats and the SC of 21 rats subjected to a severe weight-drop contusion injury were evaluated at 1, 2, 4, 6, and 12 months after injury. The axonal diameter and the myelination index (MI=axolemmal perimeter divided by myelinated fiber perimeter) were registered in the outer rim of the cord at T9 SC level using a transmission electron microscope and a digitizing computer system. The average myelinated fiber loss was 95.1%. One month after the SC, 64% of the surviving fibers were demyelinated while 12 months later, only 30% of the fibers had no myelin sheath. The MI in the control group was 0.72±0.07 (X±S.D.). In the experimental groups, the greatest demyelination was observed two months after the lesion (MI=0.90±0.03), while the greatest myelination was observed 12 months after the injury (MI=0.83±0.02). There was a statistical difference (p<0.02) in MI between 2 and 12 months which means that remyelination had taken place. Remyelination was mainly achieved because of Schwann cells. The proportion of small fibers (diameter=0.5 μm or less) considered as axon collaterals, increased from 18.45% at 1 month to 27.66% a year after the contusion. Results suggest that remyelination is not an abortive phenomenon but in fact a slow process occurring parallel to other tissue plastic phenomena, such as the emission of axon collaterals.     

Secondary spinal cord hypoperfusion of circumscribed areas after injury in rats

OBJECTIVES: The evaluation of the spatial spread of ischemia following spinal cord injury (SCI) is important for planning therapeutic strategies for secondary injury. The purpose of this study was to investigate in detail the change in regional spinal cord blood flow (rSCBF) after SCI. METHODS: Thirty-four male Wistar rats were used, for which laminectomies of the T11-13 vertebrae were performed. SCI was produced by a directed impact through a laminectomy site at the level of the Th12 using a pneumatic impact device. We measured the sequential and spatial changes of rSCBF using a laser Doppler scanning technique before and after SCI in rats not only at the injured myelomere but also at the circumferent myelomeres. SCBF mapping was carried out before and after SCI on each site. RESULTS: After SCI, the rSCBF value gradually decreased for each site for the SCI group (n=26), while it globally decreased at the epicenter. Moreover, a decrease in SCBF was observed at the caudal and rostral sites. The mean value of the %SCBF 120 minutes after SCI for each site was 63.6+/-2.3% (Th11), 74.4+/-4.5% (Th12), 75.8+/-3.2% (Th13), and was significantly lower for the rostral site compared with the caudal site (p<0.05, one-way analysis of variance). DISCUSSION: This study found that SCBF is significantly decreased not only at the injured myelomere but also at the circumferent myelomeres. Circumferentially extending ischemia after SCI is related to secondary injury after SCI. The improvement in SCBF after SCI, therefore, can be attributed to the treatment of SCI.     

Local spinal cord glucose utilization and extracellular potassium activity changes after spinal cord injury in rats

Spinal microenvironment and metabolic alterations after experimental contusional injury of the spinal cord were evaluated in the same Wistar rats. Severe spinal cord injury was made under light GOF anesthesia with a 10 g weight drop onto the exposed Th-8 spinal cord from a 10 cm height and then halothane was ceased. The author studied extracellular potassium activity ([K+]e) and DC potential for 2 hours after paraplegic spinal cord injury in conscious rats. Furthermore, at 2 hours after cord injury, local spinal cord glucose utilization (1-SCGU) was measured with quantitative autoradiographic 2-[14C] deoxy-glucose method (Sokoloff et al.). [K+]e in injured spinal cords was 59 +/- 5 (mean +/- S.E.M.) mEq at 10 min after injury and was cleared with an exponential half-life of 1 hour. At 2 hours after injury [K+]e was still high with a value of 16 +/- 1 mEq compared with 4 mEq of control animals. DC potential changes was a mirror image of that of [K+]e. DC potential changed by a mean of 10.7 mV positively from 10 min. to 2 hours after injury. 1-SCGU at the impact site was extremely low in both white and gray matters. At 6mm rostral from the impact center 1-SCGU was remarkably reduced in the gray matter, and in the lateral white matter. But at 3 mm rostral 1-SCGU was well preserved. And at 20 mm rostral there was no difference in 1-SCGU with control animals. Massive potassium efflux from the injured spinal cord to the adjacent spinal segment was clarified at this experiment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Neuroprotective effect of apigenin in rats after contusive spinal cord injury

Apigenin, a common plant flavonoid, has been extensively studied and showed a wide variety of beneficial effects. The aim of this study was to determine the therapeutic efficacy of starting apigenin treatment 3 day after spinal cord injury (SCI) in rat and to investigate the underlying mechanism. SCI was induced using the modified weight-drop method in Sprague–Dawley rats. The SCI animals were randomly assigned to five groups: sham control group, SCI model group, the methylprednisolone sodium succinate (MPSS) group, the 10 mg/kg apigenin treatment group and the 20 mg/kg apigenin treatment group. First, neuronal function after SCI was evaluated with Basso Beattie Bresnahan locomotor rating scale (BBB) and the result showed that injured animals treated with apigenin showed a significant increase in BBB scores. To explore the underlying mechanism, antioxidative effect of apigenin was assessed by measuring malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities after SCI. Apigenin treatment reversed the decrease of SOD and GSH-Px activity, and the increase of MDA level caused by SCI, suggesting its antioxidative role in response to the injury. In addition, apigenin treatment decreased serum interleukin-1β, tumor necrosis factor-α and intercellular adhesion molecule-1 release after SCI, suggesting an anti-inflammatory effect of apigenin. Finally, apigenin treatment affected the expression level of apoptosis-related gene Bax, Bcl-2 and caspase-3, which indicated its antiapoptosis role after SCI. Our data suggest that apigenin significantly promotes the recovery of rat neuronal function after SCI, which is associated with its antioxidative, anti-inflammatory and antiapoptotic properties.     

Exudation of fibronectin and albumin after spinal cord injury in rats

Summary Spinal cord of the rat was investigated immunohistochemically to detect signs of extravasation of fibronectin in animals in which the cord was subjected to different degrees of compression trauma. Immuno-histochemistry was performed after survival periods of 4 and 24h and parallel sections were incubated for albumin immunoreactivity to detect signs of breakdown of the blood-spinal cord barrier. Extravascular reaction products indicating the presence of fibronectin were found within and in the vicinity of the compression provided that bleeding had occurred in the spinal cord, i.e., in rats with severe trauma. Immunoreactive material indicating extravascular albumin was present in the traumatized region and in many segments of the cord located away from the compressed part. Such material was seen both proximal and distal to the primary injury and even in rats with a low magnitude of compression. Generally, with more severe trauma and longer survival periods extravascular albumin was more extensively distributed along the cord. No signs of fibronectin antigen were detected in spinal cord segments away from the compression even though such regions showed albumin immunoreactivity outside the vessels. The results indicate that within and close to the primary injury of compressed spinal cord exudation of fibronectin may occur from the plasma of microvessles provided that the impact is severe enough to cause intramedullary hemorrhages.Supported by grants from the Swedish Medical Research Council project nr 3020, Söderberg stiftelse, Swärds stiftelse, Hedlunds stiftelse, Thyrings stiftelse, RTP, Wallenius Line, and Åhléns stiftelse.     

香芹酚对大鼠急性脊髓损伤的保护作用

目的 探讨香芹酚对大鼠脊髓损伤（SCI）后神经功能的影响及其机制。方法 将60只雄性SD大鼠（200~250 g）随机分为5组:假手术组（n=12）、SCI组（n=12）、香芹酚组（n=36）,香芹酚组根据香芹酚剂量分为低、中、高剂量3个亚组,每亚组12只。低、中、高剂量香芹酚组SCI后30 min腹腔注射香芹酚,剂量分别为10、20、40 mg/kg,每日一次;假手术组和SCI组每日腹腔注射等量生理盐水。采用Allen法建立大鼠SCI模型;假手术组只行椎板切除手术。SCI后24、48、72 h,采用BBB评分评估大鼠神经功能;SCI后72 h,采用ELISA法检测损伤脊髓组织丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽（GSH）、过氧化氢酶（CAT）、caspase-3活性;Western-blot法检测损伤脊髓组织Bax,Bcl-2蛋白表达水平。结果 SCI后,大鼠BBB评分均明显降低（P<0.05）,损伤脊髓组织水肿指数以及MDA、caspase-3和Bax水平均明显增高（P<0.05）,而SOD、GSH、CAT、Bcl-2水平均明显降低（P<0.05）;香芹酚能明显改善大鼠BBB评分（P<0.05）,明显降低水肿指数以及MDA、caspase-3和Bax水平（P<0.05）,而显著增加CAT、SOD、GSH、Bcl-2水平（P<0.05）。结论 香芹酚可通过减轻脊髓水肿、抑制氧化应激反应以及抗凋亡作用而对SCI大鼠发挥神经保护作用。     

Glutamate receptor subunit expression after spinal cord injury in young rats

To investigate the possibility that glutamate receptor levels in the spinal cord are altered following injury to young rats, we used a previously characterized model of spinal cord contusion that produces a reliable injury in rats at postnatal day 14-15. Quantitative Western blot analysis was used to measure relative amounts of protein for several glutamate receptor subunits acutely (24 h) and chronically (28 days) after spinal cord injury (SCI). Acutely after injury significant decreases were observed in the GluR1, GluR2, and GluR4 subunits of the alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionate (AMPA) receptor, and the NR2A and NR2B subunits, but not the NR1 subunit, of the N-methyl-d-aspartate (NMDA) receptor. However, 28 days after injury only one subunit (GluR4) was shown to be altered. These widespread changes that occur acutely in receptor subunit expression may be an attempt to protect cells from glutamate-induced death. The injured spinal cord in these young animals, however, appears to have the capacity to regulate receptor subunit levels to normal within a month of injury.     

Muscle after spinal cord injury

The morphological and contractile changes of muscles below the level of the lesion after spinal cord injury (SCI) are dramatic. In humans with SCI, a fiber‐type transformation away from type I begins 4–7 months post‐SCI and reaches a new steady state with predominantly fast glycolytic IIX fibers years after the injury. There is a progressive drop in the proportion of slow myosin heavy chain (MHC) isoform fibers and a rise in the proportion of fibers that coexpress both the fast and slow MHC isoforms. The oxidative enzymatic activity starts to decline after the first few months post‐SCI. Muscles from individuals with chronic SCI show less resistance to fatigue, and the speed‐related contractile properties change, becoming faster. These findings are also present in animals. Future studies should longitudinally examine changes in muscles from early SCI until steady state is reached in order to determine optimal training protocols for maintaining skeletal muscle after paralysis. Muscle Nerve, 2009     

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.     

Alterations in protein expression patterns of spinal peroxisome proliferator-activated receptors after spinal cord injury

ABSTRACT

Objectives: Peroxisome proliferator-activated receptors (PPARs) control wound healing processes in damaged tissues. PPAR agonists have neuroprotective effects in spinal cord injury (SCI); however, isotype-specific roles of PPARs are not well understood. Therefore, we evaluated protein expression changes for three isotypes of PPARs at different time points and locations relative to the epicenter after SCI in rats.

Methods: A 10-g rod was dropped on the spinal cord which located at the T10 vertebra of rats from a height of 6.25, 12.5, or 50 mm using New York University impactor. We collected the spinal cord at 6, 12, 24, and 72 h and 1, 3, and 5 weeks after SCI. The protein expression of PPARs was analyzed using western blot.

Results: The protein expression of PPAR-α declined gradually up to 5 weeks at the epicenter. PPAR-β/δ expression increased from 3 days to 5 weeks at the caudal region, but decreased at the epicenter in the severe injury group. PPAR-γ expression increased significantly at all regions in all three injury groups up to 5 weeks after SCI and increased to a greater extent in the severe injury group. In addition, PPAR-β/δ controlled protein expression of PPAR-α positively, and -γ negatively.

Conclusions: The present results suggest that different PPAR isotypes have varied protein expression patterns at the epicenter and in adjacent regions after SCI. Our results suggest that PPARs may have overlapping but distinct roles. These findings will be useful for further studies investigating PPARs in neurological disorders including SCI.     

GRP94 (94 kDa glucose-regulated protein) suppresses ischemic neuronal cell death against ischemia/reperfusion injury

The 94 kDa glucose-regulated protein (GRP94), the endoplasmic reticulum (ER) resident molecular chaperone, has a role in cell death due to endoplasmic reticulum stress (ER stress). Here, we report that expression of GRP94 was increased in human neuroblastoma cells (SH-SY5Y (SY5Y) cells) exposed to hypoxia/reoxygenation (H/R). H/R mediated death of SY5Y cells was associated with the activation of major cysteine proteases, caspase-3 and calpain, along with an elevated intracellular calcium concentration. Pretreatment with adenovirus-mediated antisense GRP94 (AdGRP94AS) led to reduced viability of SY5Y cells after being subjected to H/R compared with wild-type cells or cells with adenovirus-mediated overexpression of GRP94 (AdGRP94S). These results indicate that suppression of GRP94 is associated with accelerated apoptosis and that expression of GRP94 (as a stress protein) suppresses oxidative stress-mediated neuronal death and stabilizes calcium homeostasis in the ER. We also used gerbils with transient forebrain ischemia to study the role of GRP94 in vivo. Neurons with adenovirus-mediated overexpression of GRP94 were resistant to ischemic damage. These results confirmed that GRP94 could suppress ischemic injury to neurons, suggesting that gene transfer of GRP94 into the brain may have therapeutic potential in the treatment of cerebrovascular disease.     

脊髓损伤模型大鼠神经胶质细胞增殖与胶质纤维酸性蛋白的表达

背景：星形胶质细胞可以通过细胞裂解释放各种神经营养因子,并可促进损伤脊髓的修复。 目的：观察脊髓损伤模型大鼠神经胶质纤维酸性蛋白的表达及对其后肢功能恢复的影响。 方法：将SD大鼠采用Allen's法撞击T9~10节段致脊髓损伤,造模成功后蛛网膜下腔移植骨形态发生蛋白7,并设置仅蛛网膜下腔移植His蛋白的正常SD大鼠做对照。用BBB评分法评估两组大鼠后肢的运动功能,用免疫组织化学染色法和Western-blot法观察各组神经胶质纤维酸性蛋白的表达。 结果与结论：BBB评分结果显示,模型组大鼠脊髓损伤后下肢功能自行恢复率达68%。模型组脊髓损伤3和7 d,损伤区域神经胶质纤维酸性蛋白表达逐渐增加(P < 0.05),随后逐渐下降,于脊髓损伤28 d后逐渐恢复到对照组水平(P > 0.05)。脊髓损伤后1~14 d两组胶质纤维酸性蛋白表达逐渐升高(P > 0.05)。结果证实,脊髓损伤后蛛网膜下腔移植骨形态发生蛋白7可诱导星形胶质细胞增殖,神经胶质纤维酸性蛋白的表达增强,进而促进脊髓损伤大鼠后肢功能的恢复。     

Neuroprotective effect of estrogen after chronic spinal cord injury in ovariectomized rats

BACKGROUND: At present, there is still lack of effective drugs for chronic spinal cord injury, whereas it is found recently that estrogen has a neuroprotective effect on brain and spinal cord injuries. OBJECTIVE: To observe the effect of estrogen on the apoptosis of nerve cells after gradual chronic spinal cord injury in ovariectomized rats. DESIGN: A randomized controlled animal trial. SETTING: Institute of Orthopaedics, the Second Hospital of Lanzhou University. MATERIALS: Sixty-five female Wistar rats of common degree, weighing 220–250 g, were provided by the experimental animal center of Lanzhou University. The rats were randomly divided into sham-operated group (n =5), estrogen-treated group (n =30) and saline control group (n =30), and the latter two groups were observed at 1, 3, 7, 14, 28 and 60 days respectively, and 5 rats for each time point. METHODS: All the rats were treated with bilateral oophorectomy 2 weeks before the experiment. T10 vertebral lamina was revolved into using plastic screw. The spinal canal impingement was not induced initially. After that, the original incision was opened to expose the screw every 7–10 days. MAIN OUTCOME MEASURES: The apoptosis and Caspase-3 positive cells in the damaged spinal cord were detected using terminal deoxynucleotidal transferase-mediated dUTP-biotin nick end labeling (TUNEL) method and Caspase-3 immunohistochemical staining at 1, 3, 7, 14, 28 and 60 days after chronic spinal cord injury respectively. RESULTS: Totally 65 rats were used, and the deleted ones during the experiment were supplemented by others. Changes of Caspase-3 expression after spinal cord injury: In the sham-operated group, only a small amount of Caspase-3 proteins were observed in the rat spinal cord, mainly located in motor neurons of spinal cord anterior horn. In the estrogen-treated group and saline control group, positive cells expressed occasionally at 1 day postoperatively, began to increase obviously at 7 days after injury, strongly expressed at 14 and 28 days, but decreased at 60 days, mainly located in the neurons of spinal cord gray matter anterior horn, and they expressed fewer in the motor neurons and white matter of ventral horn, and there were obvious differences between the estrogen-treated group and saline control group at 7, 14, 28 and 60 days (P < 0.05). CONCLUSION: Estrogen can reduce the apoptosis of nerve cells and promote the recovery of neurological function following gradual chronic spinal cord injury.     

Expression of CDc6 after acute spinal cord injury in adult rats

The cell division cycle 6 (CDc6) protein has been primarily investigated as a component of the pre-replicative complex for the initiation of DNA replication. Some studies have shown that CDc6 played a critical role in the development of human carcinoma. However, the expression and roles of CDc6 in the central nervous system remain unknown. We have performed an acute spinal cord injury (SCI) model in adult rats and investigated the dynamic changes of CDc6 expression in spinal cord. Western blot have found that CDc6 protein levels first significantly increase, reach a peak at day 3, and then gradually return to normal level at day 14 after SCI. Double immunofluorescence staining showed that CDc6 immunoreactivity was found in neurons, astrocytes, and microglia. Additionally, colocalization of CDc6/active caspase-3 has been detected in neurons and colocalization of CDc6/proliferating cell nuclear antigen has been detected in astrocytes and microglial. In vitro, CDc6 depletion by short interfering RNA inhibits astrocyte proliferation and reduces cyclin A and cyclin D1 protein levels. CDc6 knockdown also decreases neuronal apoptosis. We speculate that CDc6 might play crucial roles in CNS pathophysiology after SCI.     

Tamoxifen对大鼠脊髓损伤后神经元凋亡的影响

目的探讨Tamoxifen对大鼠脊髓损伤后神经元凋亡的影响,阐明其可能的神经保护机制。方法采用改良Allen法建立大鼠脊髓挫伤模型,并将大鼠随机分为假手术组、对照组和干预组,采用免疫荧光染色和TUNEL双标技术检测各组神经元的凋亡变化。结果假手术组中神经元凋亡数目较少,脊髓损伤后损伤灶周边凋亡的神经元数目明显增多(P<0.01),给予Tamoxifen干预后神经元凋亡显著降低(P<0.05)。结论Tamoxifen可以减轻大鼠脊髓损伤后的神经元凋亡,从而发挥神经保护作用。