The ameliorating effect of dantrolene on the morphology of urinary bladder in spinal cord injured rats

In animal models of spinal cord injury (SCI), the urinary bladder can undergo significant structural and physiological alterations. Dantrolene has been shown to be neuroprotective by reducing neuronal apoptosis after SCI. Furthermore, in addition to its anti-inflammatory and antioxidant properties, it appears to have a beneficial action on voiding, once this drug acts on the external urethral sphincter relaxation. In the present study, we investigated the effects of dantrolene on urinary bladder injury that follows experimental SCI. Forty-six male Wistar rats were laminectomized at T13, and a compressive trauma was performed to induce SCI. After euthanasia, the urinary bladder was removed for gross and histological evaluation. Traumatized animals showed urinary retention with severe hemorrhagic cystitis. Injured animals treated with dantrolene had less bladder hemorrhage and inflammatory infiltrate than those treated with placebo (p<0.05). Our results demonstrate that dantrolene may protect against urinary bladder lesions that follow SCI. Treating spinal cord-injured patients with this agent may be a promising additional therapeutic strategy to alleviate the accompanying inflammatory process. The results of the current study show that dantrolene has protective effects on spinal cord contusion-induced urinary bladder injury. The impaired integrity of bladder morphology was ameliorated by dantrolene treatment.     

Effects of dantrolene on apoptosis and immunohistochemical expression of NeuN in the spinal cord after traumatic injury in rats

Dantrolene has been shown to be neuroprotective by reducing neuronal apoptosis after brain injury in several animal models of neurological disorders. In this study, we investigated the effects of dantrolene on experimental spinal cord injury (SCI). Forty-six male Wistar rats were laminectomized at T13 and divided in six groups: GI (n = 7) underwent SCI with placebo and was euthanized after 32 h; GII (n = 7) underwent laminectomy alone with placebo and was euthanized after 32 h; GIII (n = 8) underwent SCI with dantrolene and was euthanized after 32 h; GIV (n = 8) underwent SCI with placebo and was euthanized after 8 days; GV (n = 8) underwent laminectomy alone with placebo and was euthanized after 8 days; and GVI (n = 8) underwent SCI with dantrolene and was euthanized after 8 days. A compressive trauma was performed to induce SCI. After euthanasia, the spinal cord was evaluated using light microscopy, TUNEL staining and immunochemistry with anti-Caspase-3 and anti-NeuN. Animals treated with dantrolene showed a smaller number of TUNEL-positive and caspase-3-positive cells and a larger number of NeuN-positive neurons, both at 32 h and 8 days (P ≤ 0.05). These results showed that dantrolene protects spinal cord tissue after traumatic SCI by decreasing apoptotic cell death.     

Effect of 21-aminosteroid on extracellular energy-related metabolites and amino acids after compression injury of rat spinal cord

We evaluated in a rat model of severe spinal cord compression the effect of the 21-aminosteroid tirilazad on extracellular levels of energy metabolites and amino acids, until 3 h after injury. The compound was given i.v. 30 min before injury (3 mg/kg) and hourly thereafter (1.5 mg/kg). The findings were compared with previously reported effects of methylprednisolone. Both treated and untreated rats with spinal cord compression showed, at 10 min after injury, a five-to sixfold elevation of extracellular lactate above the preinjury level. There was no significant difference for lactate, pyruvate or lactate/pyruvate ratio between the treated and untreated injured groups at any time point after trauma. Glutamate was significantly elevated both in treated and untreated injured rats for 20 min after trauma. The mean glutamate level was lower in animals treated with 21-aminosteroid. However, there was no statistically significant difference between the treated and untreated rats at any time after trauma. There was no statistically significant difference between the groups for aspartate, serine, glutamine, histidine, glycine, threonine, taurine, alanine and tyrosine. In conclusion our findings indicate that, in the injured spinal cord, methylprednisolone and the 21-aminosteroid have differences and similarities, regarding their effects on energy and amino acid metabolism. The lowering of the lactate and arginine levels early after trauma seen with methylprednisolone pretreatment was absent after 21-aminosteroid pretreatment. However, the mean extracellular level of glutamate was lower with both methyl-prednisolone and 21-aminosteroid after injury, although the difference was not statistically significant between treated and untreated rats.     

Therapeutic time window for methylprednisolone in spinal cord injured rat.

Recent clinical trials have reported that methylprednisolone sodium succinate administered within 8 hours improves neurological recovery in human spinal cord injury (SCI). Methylprednisolone, however, was ineffective and possibly even deleterious when given more than 8 hours after injury. This finding suggests that a therapeutic time window exists in spinal cord injury. In order to determine the doses, durations and timing of methylprednisolone treatment for optimal neuroprotection, a single or two bolus dose of methylprednisolone (30 mg/kg) was administered at 10, 30, 120, 150 and 240 min. after three graded spinal cord injury. The primary outcome measure was 24-hour spinal cord lesion volumes estimated from spinal cord Na+ and K+ shifts. A single 30 mg/kg dose of methylprednisolone at 10 min. after injury significantly reduced 24-hour lesion volumes in injured rat spinal cords. However, any other methylprednisolone treatment starting 30 min. or more after injury had no effect on 24-hour lesion volumes compared to the vehicle control group. Moreover, delayed treatment increased lesion volumes in some cases. These results suggest that the NYU SCI model has a very short therapeutic window.     

Histopathological investigation of neuroprotective effects of Nigella sativa on motor neurons anterior horn spinal cord after sciatic nerve crush in rats

The aim of this study was designed to evaluate the possible protective effects of Nigella sativa (NS) on the neuronal injury in the sciatic nerve of rats. The rats were randomly allotted into one of the three experimental groups: A (control), B (only trauma) and C (trauma and treated with NS); each group contain 10 animals. Sciatic nerve injury was performed by placing an aneurysm clip on the left leg. Rats were neurologically tested over 24 h after trauma. The rats in NS-treated group was given NS (in a dose of 400 mg/kg body weight) once a day orally for 30 days starting just after trauma. Control and untreated (only trauma) rats were injected with the same volume of isotonic NaCl as the treated animals that received NS. Tissue samples were obtained for histopathological investigation. To date, no histopathological changes of neurodegeneration in the sciatic nerve after trauma in rats by NS treatment have been reported. Results showed in the group B (only trauma), the neurons of sciatic nerve tissue became extensively dark and degenerated with picnotic nuclei. Treatment of NS markedly reduced degenerating neurons after trauma and the distorted nerve cells were mainly absent in the NS-treated rats. The morphology of neurons in groups treated with NS was well protected, but not as neurons of the control group. The number of neurons in sciatic nerve tissue of group B (only trauma) was significantly less than both control and treated with NS groups. The morphology of neurons revealed that the number of neurons were significantly less in group B compared to control (P < 0.001) and group C (P < 0.01) rats’ motor neurons anterior horn spinal cord tissue. We conclude that NS therapy causes morphologic improvement on neurodegeneration in sciatic nerve after trauma in rats.     

Pregabalin as a neuroprotector after spinal cord injury in rats: biochemical analysis and effect on glial cells

As one of trials on neuroprotection after spinal cord injury, we used pregabalin. After spinal cord injury (SCI) in rats using contusion model, we observed the effect of pregabalin compared to that of the control and the methylprednisolone treated rats. We observed locomotor improvement of paralyzed hindlimb and body weight changes for clinical evaluation and caspase-3, bcl-2, and p38 MAPK expressions using western blotting. On histopathological analysis, we also evaluated reactive proliferation of glial cells. We were able to observe pregabalin's effectiveness as a neuroprotector after SCI in terms of the clinical indicators and the laboratory findings. The caspase-3 and phosphorylated p38 MAPK expressions of the pregabalin group were lower than those of the control group (statistically significant with caspase-3). Bcl-2 showed no significant difference between the control group and the treated groups. On the histopathological analysis, pregabalin treatment demonstrated less proliferation of the microglia and astrocytes. With this animal study, we were able to demonstrate reproducible results of pregabalin's neuroprotection effect. Diminished production of caspase-3 and phosphorylated p38 MAPK and as well as decreased proliferation of astrocytes were seen with the administration of pregabalin. This influence on spinal cord injury might be a possible approach for achieving neuroprotection following central nervous system trauma including spinal cord injury.     

大剂量甲基强的松龙冲击治疗成人急性脊髓损伤疗效的Meta分析

背景：一些随机对照研究试图回答大剂量甲基强的松龙冲击治疗成人急性脊髓损伤的疗效优劣问题,得出结论各不相同。 目的：大剂量甲基强的松龙冲击治疗成人急性脊髓损伤的疗效Meta分析。 方法：计算机检索PubMed、Embase、Cochrane图书馆及中国生物医学数据库、维普信息数据库、万方数据库,手工检索相关的中英文骨科杂志。收集大剂量甲基强的松龙冲击治疗成人急性脊髓损伤的对照试验,并评价纳入研究的方法学质量。统计软件用Cochrane协作网提供的RevMan 5.0。 结果与结论：共纳入9个临床对照试验。Meta分析结果表明,与传统治疗方案相比,甲基强的松龙在给药后24 h患者的神经功能恢复、肺部感染率、胃肠道反应发生率较高,而在泌尿系感染率、术后伤口不愈合率、应激性溃疡发生率方面与传统治疗差异无显著性意义。提示大剂量甲基强的松龙冲击治疗成人急性脊髓损伤时,对神经功能的恢复有较好的效果,但是有较高的肺部感染和胃肠道反应的发生,所以在今后的治疗过程中要尽可能的避免肺部感染和胃肠道反应的发生。 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

大剂量甲基强的松龙不能通过溶酶体途径保护损伤早期的脊髓神经

背景：Cathepsis家族是否参与脊髓损伤早期的病理过程以及大剂量甲基强的松龙是否通过溶酶体机制发挥神经保护作用目前尚不清楚。 目的：检测Cathepsin基因家族在脊髓损伤早期的表达和大剂量甲基强的松龙干预后的变化,明确大剂量甲基强的松龙是否通过调节溶酶体凋亡途径发挥神经保护作用。 方法：9只日本大耳兔随机分为3组：模型组和药物组进行椎板切除后采用Allen法建立急性脊髓损伤模型,药物组在造模后2 h按人-兔等效剂量给予大剂量甲基强的松龙冲击治疗,对照组仅进行椎板切除。造模后8 h处死实验动物,取脊髓组织,采用Trizol法提取总RNA,用9张Agilent 兔子全基因4*44K芯片进行检测。采用GeneSpring 10.0软件,以P < 0.05 且倍数变化(FC)≥2筛选出差异表达基因。 结果与结论：成功建立脊髓损伤的动物模型并获得相应的组织标本。9组标本总RNA的质量均能满足基因芯片检测要求。基因芯片结果显示：在10个Cathepsin基因家族成员中,仅Cathepsin Z和proathepsin E 在创伤后呈现差异性表达,Cathepsin C、D、F、K、L、S和W表达均无差异。甲基强的松龙冲击治疗后Cathepsin家族基因表达均无差异(在药物组与模型组的比较)。提示Cathepsin Z和E参与了脊髓损伤早期凋亡过程,但大剂量甲基强的松龙并不能通过溶酶体凋亡途径发挥神经保护作用。     

Repeated Baclofen treatment ameliorates motor dysfunction,suppresses reflex activity and decreases the expression of signaling proteins in reticular nuclei and lumbar motoneurons after spinal trauma in rats

The interruption of supraspinal input to the spinal cord leads to motor dysfunction and the development of spasticity. Clinical studies have shown that Baclofen (a GABA_B agonist), while effective in modulating spasticity is associated with side-effects and the development of tolerance. The aim of the present study was to assess if discontinued Baclofen treatment and its repeated application leads antispasticity effects, and whether such changes affect neuronal nitric oxide synthase (nNOS) in the brainstem, nNOS and parvalbumin (PV) in lumbar α-motoneurons and glial fibrillary acidic protein in the ventral horn of the spinal cord. Adult male Wistar rats were exposed to Th9 spinal cord transection. Baclofen (30 mg/b.w.) diluted in drinking water, was administered for 6 days, starting at week 1 after injury and then repeated till week 4 after injury. The behavior of the animals was tested (tail-flick test, BBB locomotor score) from 1 to 8 weeks. Our results clearly indicate the role of nitric oxide, produced by nNOS in the initiation and the maintenance of spasticity states 1, 6 and 8 weeks after spinal trauma. A considerable decrease of nNOS staining after Baclofen treatment correlates with improvement of motor dysfunction. The findings also show that parvalbumin and astrocytes participate in the regulation of ion concentrations in the sub-acute phase after the injury.     

Immunohistochemical study of apoptosis in the cells of experimental injured spinal cord

We studied the temporal and spatial profile of apoptosis following acute spinal cord (SC) injury in rats and influence of chicken yolk transplantation on the programmed cell death. 18 female rats were subjected to complete SC transsection with removal of three millimeters of the SC at the level of the ninth thoracic vertebra. The gap was filled with denaturated chicken yolk in 9 animals. 9 control rats had no transplantation. Temporal and spatial course of apoptosis was estimated in longitudinal sections of the SC by TUNEL assay technique 4 hours, 3 days, 2 weeks, 40 days and 3 months after the injury. Apoptosis occurred through all posttraumatic period with its peak 40 days after the injury and decreased slowly to the minimal level by the third month. Apoptotic cells appeared near the site of the injury immediately after the trauma along the cord several hours later. Apoptosis involved only glial cells, neurons had no apoptotic signs. Suppression of apoptosis occurred in the yolk transplantation group and was accompanied by greater number of neuronal and glial survivals. Thus, apoptotic glial death after transsection of the SC in rats occurred mainly for the first eight weeks along the whole spinal cord.     

鼓室注射甲泼尼龙琥珀酸钠联合糖皮质激素治疗 突发性耳聋的疗效

目的 探讨鼓室注射甲泼尼龙琥珀酸钠联合糖皮质激素治疗突发性耳聋的临床疗效。方法 选择2015年11月~2018年9月我院收治的突发性耳聋患者86例,随机分成联合组和对照组,每组43例。对照组给予糖皮质激素治疗,联合组在对照组基础上给予鼓室注射甲泼尼龙琥珀酸钠联合治疗,比较两组临床疗效,治疗前后不同频率听力及不良反应发生率。结果 联合组总有效率为97.62%,高于对照组的76.74%,差异有统计学意义（P＜0.05）。治疗后,联合组500 Hz、1000 Hz、2000 Hz、4000 Hz听力优于对照组,差异有统计学意义（P＜0.05）。联合组不良反应总发生率为2.33%,低于对照组的9.30%,差异有统计学意义（P＜0.05）。结论 鼓室注射甲泼尼龙琥珀酸钠联合糖皮质激素可有效治疗突发性耳聋,改善患者听力,且不良反应较少。     

A novel biodegradable implant for neuronal rescue and regeneration after spinal cord injury

After spinal cord injury, the severed neuronal pathways fail to regenerate spontaneously. This study describes a biodegradable implant using poly-beta-hydroxybutyrate (PHB) fibers as carrier scaffold for matrix components and cell lines supporting neuronal survival and regeneration after spinal cord injury. After cervical spinal cord injury in adult rats, a graft consisting of PHB fibers coated with alginate hydrogel + fibronectin was implanted in the lesion cavity. In control groups, PHB was omitted and only alginate hydrogel or fibronectin, or their combination, were used for grafting. In addition, comparisons were made with animals treated intrathecally after spinal cord injury with the neurotrophic factors BDNF or NT-3. The neurons of the rubrospinal tract served as experimental model. In untreated animals, 45% of the injured rubrospinal neurons were lost at 8 weeks postoperatively. Implantation of the PHB graft reduced this cell loss by 50%, a rescuing effect similar to that obtained after treatment with BDNF or NT-3. In the absence of PHB support, implants of only alginate hydrogel or fibronectin, or their combination, had no effect on neuronal survival. After addition of neonatal Schwann cells to the PHB graft, regenerating axons were seen to enter the graft from both ends and to extend along its entire length. These results show that implants using PHB as carrier scaffold and containing alginate hydrogel, fibronectin and Schwann cells can support neuronal survival and regeneration after spinal cord injury     

督脉电针与神经干细胞移植联合应用促进脊髓全横断大鼠受损伤的神经元存活及其轴突再生

目的探讨督脉电针与神经干细胞移植联合应用对脊髓全横断大鼠受损伤的神经元存活及其轴突再生的影响。方法将对照组、神经干细胞移植组、督脉电针组和督脉电针＋神经干细胞移植组的成年大鼠胸10脊髓段做全横断损伤;其中神经干细胞移植组和电针神经干细胞组在损伤处移植神经干细胞。电针组和电针神经干细胞移植组在术后开始接受督脉电针治疗。所有动物存活67d。结果1．电针神经干细胞移植组脊髓损伤处的去甲肾上腺素能、5-羟色胺受体、降钙素基因相关肽能和生长相关蛋白-43阳性染色的4种神经纤维均明显多于其他几组。2．电镜下可观察到脊髓横断处有再生的神经纤维穿越,在电针神经干细胞移植组尤为明显。3．大脑体感运动区皮质和中脑红核受损伤的神经元存活数量也多于其他几组,一些神经元的再生神经纤维可能穿越横断处,进入尾端脊髓组织。结论督脉电针与神经干细胞移植联合应用能促进脊髓全横断大鼠受损伤的神经元存活及其轴突再生。     

Effects of methylprednisolone and ganglioside GM-1 on a spinal lesion: a functional analysis

OBJECTIVES: The pharmacological effects of methylprednisolone (MP) and ganglioside GM-1 on spinal injuries have been thoroughly investigated, but only a few studies have evaluated the interaction between these two drugs. METHODS: Twenty-four Wistar rats were subjected to contusive injury of the spinal cord produced by the NYU system. These animals were divided into four groups: group I was injected with MP; group II was injected with GM-1; group III was injected with MP together with GM-1; and group control received physiological serum. The animals were evaluated with regard to their recovery of locomotive function by means of the BBB test on the second, seventh and fourteenth days after receiving the contusive injury to the spinal cord. They were sacrificed on the fourteenth day. RESULTS: This study demonstrated that the MP and GM-1 groups presented functional results that were better than those of the control group, although the enhanced recovery of group II (GM-1) relative to the control group was not statistically significant (p>0.05). The most notable recovery of locomotive function was observed in the group that received MP alone (p<0.05). The group that received MP together with GM-1 presented results that were better than those of the control group (p<0.05). CONCLUSION: Administration of methylprednisolone alone or with GM-1 was shown to be effective for recovery of locomotive function. Combined administration of these drugs resulted in better outcomes than administration of methylprednisolone alone.     

Transplantation of undifferentiated and induced human exfoliated deciduous teeth-derived stem cells promote functional recovery of rat spinal cord contusion injury model

Regarding both the neural crest origin and neuronal potential of stem cells from human exfoliated deciduous teeth (SHED), here, we assessed their potential in addition to neural induced SHED (iSHED) for functional recovery when transplanted in a rat model for acute contused spinal cord injury (SCI). Following transplantation, a significant functional recovery was observed in both groups relative to the vehicle and control groups as determined by the open field locomotor functional test. We also observed that animals that received iSHED were in a better state as compared with the SHED group. Immunohistofluorescence evaluation 5 weeks after transplantation showed neuronal and glial differentiation and limited proliferation in both groups. However, myelin basic protein and chondroitin sulfate proteoglycan NG2-oligodendrocyte markers-were increased and glial fibrillary acidic protein-astrocyte marker-was decreased in the iSHED group in comparison with the SHED group. These findings have demonstrated that transplantation of SHED or its derivatives could be a suitable candidate for the treatment of SCI as well as other neuronal degenerative diseases.     

Muscle damage induced by running training during recovery from hindlimb suspension: the effect of dantrolene sodium

We examined the extent of morphological alterations and the myosin heavy chain (MHC) distribution in the rat soleus muscle after a 4-week period of spontaneous recovery or retraining after hindlimb suspension (HS). Moreover, we tested the hypothesis that dantrolene sodium, which affects the flux of calcium over the sarcoplasmic reticulum membrane, was able to attenuate muscle damage. Three groups of rats were submitted to 3 weeks of HS, followed by either 4 weeks of unrestricted cage activity (HC, n?=?7), or running training for the same period and were compared to age-matched animals (C, n?=?8). Trained rats were treated with either placebo or dantrolene sodium (HTP, HTD, n?=?8 each, respectively). Four weeks after HS recovery, the percentage of myofibres with internal nuclei (%in) was determined by histological staining with hematoxylin and eosin. %in was affected by the individual rat (P?P?P?r?=??0.65, P?相似文献   

Glucocorticoid and antibiotic effects on hepatic microcirculation and associated host responses in lethal gram-negative bacteremia.

Liver changes and associated host responses were evaluated in four groups of male rats, weighing 300 +/- 20 gm., which received intravenous injection of 2.2 times 10(9) live Escherichia coli. This bolus was given either without additional treatment (group A) or prior to the following regimens: intramuscular injection of gentamicin sulfate, 5 mg. per kg. (group B); intravenous injection of methylprednisolone sodium succinate, 40 mg. per kg. (group C); and intramuscular injection of gentamicin immediately after methylprednisolone sodium succinate treatment (group D). Rats given injections of saline or methylprednisolone sodium succinate served as controls. Survival rates at 10 and 20 hours were 25 per cent and 4 per cent for group A; 44 per cent and 28 per cent for group B; 94 per cent and 70 per cent for group C; 98 per cent and 98 per cent for group D, respectively. In rats of groups A and B, killed at 1, 2, 4, and 6 hours, progressive liver changes included intravascular sequestration of rapidly degranulating leukocytes, fibrinous deposits, and platelet aggregates in sinusoids as well as in spaces of Disse adjacent to subendothelial collagen, and extensive Kupffer cell disruption in association with severe midzonal necrosis. These alterations were accompanied by progressive hypoglycemia and elevations of serum enzymes, glutamic pyruvic transaminase, lactate dehydrogenase, and glutamic oxaloacetic transaminase. Hematologic studies revealed that E. coli bacteremia results in rapid leukopenia and disseminated intravascular coagulation primarily due to activation of the intrinsic coagulation pathway. All above reactions were delayed and markedly reduced in rats treated with methylprednisolone sodium succinate. The results indicate that antibiotic treatment of lethal, Gram-negative bacteremia is effective only in conjunction with early steroid treatment. The protective effects of glucocorticoids on the liver microcirculation and polymorphonuclear leukocytes appear to play a basic role in preventing the early development of disseminated intravascular coagulation, hepatocellular necrosis, and associated major host responses, thereby attenuating lethality of gram-negative septic shock.     

控释神经营养因子与细胞移植减少损伤脊髓的胶质瘢痕

背景：前期研究发现控释胶质细胞源性神经营养因子与骨髓间充质干细胞源神经元样细胞联合移植可有效促进猕猴脊髓损伤后运动功能和感觉功能的恢复。 目的：观察控释胶质细胞源性神经营养因子联合骨髓间充质干细胞源神经元样细胞移植抑制猴脊髓损伤后胶质瘢痕形成的作用是否优于单纯细胞移植。 方法：取12只恒河猴,采用改良Allen氏法制作急性重度脊髓损伤模型,随机数字表法分为3组,实验组以控释胶质细胞源性神经营养因子联合自体骨髓间充质干细胞源神经元样细胞移植修复,对照组以自体骨髓间充质干细胞源神经元样细胞移植修复,空白对照组以磷酸盐缓冲液修复。修复后5个月,取出脊髓组织制成石蜡标本,应用免疫组织化学染色显示胶质瘢痕的形态特征、构成特点及瘢痕中神经纤维的再生情况,检测胶质瘢痕面积及胶质纤维酸性蛋白染色的平均吸光度值。 结果与结论：脊髓损伤部位胶质瘢痕由混合性增生的星形胶质细胞和组织细胞构成。空白对照组脊髓胶质瘢痕累及范围广,星形胶质细胞增生显著,神经丝蛋白免疫组织化学染色阴性,胶质瘢痕面积、胶质纤维酸性蛋白染色平均吸光度值高于实验组与对照组(P < 0.05);实验组、对照组脊髓胶质瘢痕累及范围较局限,神经丝蛋白免疫组织化学染色显示有少量神经纤维通过瘢痕区,并且实验组胶质瘢痕面积、胶质纤维酸性蛋白染色平均吸光度值低于对照组(P < 0.05)。结果表明,控释胶质细胞源性神经营养因子联合骨髓间充质干细胞源性神经元样细胞移植可更强抑制脊髓损伤后胶质瘢痕的形成。     

大剂量甲基强的松龙对大鼠急性损伤脊髓Nogo-A表达量影响的研究

目的：研究大剂量甲基强的松龙对急性脊髓损伤大鼠脊髓Nogo-A蛋白表达量的影响。方法：采用allen’s打击方法，将大鼠分为正常组、急性脊髓损伤组（对照组）和急性脊髓损伤＋大剂量MP组，损伤大鼠Tg-T10节段，分别于术后3、7、14d取受损节段大鼠脊髓，运用Western-blot方法测定各时相点Nogo-A表达量及其变化，并以HE染色和免疫组化染色对受损脊髓进行形态学观察。结果：Nogo-A蛋白在各组大鼠脊髓组织中均呈阳性表达，损伤后对照组与MP组各个时相点Nogo-A表达均显著高于正常组（P〈0.05），7d时最高，后逐渐下降，但14d的表达量仍高于正常组。其中大剂量MP组与对照组在各个时间点的表达量具有显著差异（P〈0．05），MP组在各个时间点的表达量显著低于对照组。结论：Nogo-A是SCI后脊髓神经纤维再生的主要抑制因子，大剂量MP对Nogo-A的表达具有明显的抑制作用。     

成年大鼠脊髓完全性横断后星形胶质细胞的时空分布及其变化

本研究以成年大鼠脊髓完全性横断模型研究反应性胶质细胞的时空分布和变化。将30只成年Wistar大鼠随机分为5组:正常对照组,T9横断伤1周、2周、4周和8周组,每组6只。利用免疫组织化学方法及图像分析系统对各组动物脊髓内星形胶质细胞的时空分布和变化进行观察和分析。结果显示:脊髓横断组胶质纤维酸性蛋白(GFAP)阳性的星形胶质细胞数目较正常对照组明显增加(P<0.05);距损伤近侧端较距损伤远侧端的GFAP阳性星形胶质细胞数目增加显著(P<0.05);脊髓横断组髓磷脂碱性蛋白(MBP)阳性的少突胶质细胞数目的时间及空间分布与正常对照组相比无统计学差异(P>0.05)。实验结果提示,星形胶质细胞是胶质瘢痕的主要成分,而少突胶质细胞在瘢痕形成过程中并非是反应活跃的成分。