转染绿色荧光蛋白的神经干细胞移植于半横断脊髓损伤处的体内外分化研究

目的 观察转染绿色荧光蛋白(GFP)的大鼠脊髓神经干细胞移植于半横断脊髓损伤处的体内外分化情况.方法 将表达GFP的慢病毒载体转染胎鼠脊髓神经干细胞,体外用10%胎牛血清诱导分化.转染后的神经干细胞与PLGA支架移植于大鼠半横断脊髓损伤处,术后1个月和3个月取材,行GFAP、NF和CNP免疫荧光染色.结果 转染GFP的神经干细胞球表达强烈的绿色荧光,体外分化可见GFAP/GFP、NF/GFP和CNP/GFP双阳性细胞,GFAP/GFP双阳性细胞明显多于其他两种.移植后3个月,GFP阳性细胞在脊髓内明显减少,可见少数GFAP/GFP和CNP/GFP舣阳性细胞,未见NF/GFP双阳性细胞.结论 转染GFP的神经干细胞可在体外增殖和分化,但大部分分化成胶质细胞.移植于急性期脊髓损伤处的神经干细胞不被诱导分化成神经元样细胞,可被诱导分化成神经胶质细胞.     

成年大鼠脊髓损伤后损伤区血管变化及其与星形胶质细胞的关系

目的研究成年大鼠脊髓损伤后损伤区内血管的变化及其与星形胶质细胞的关系。方法通过单宁酸-氯化铁灌注，结合形态学与免疫组织化学方法，观察正常大鼠脊髓以及挤压损伤后0h、24h、72h．1周、2周、4周时的血管形态及其与星形胶质细胞的关系。结果正常脊髓血管形态清晰，可见胶质纤维酸性蛋白（GFAP）免疫反应阳性细胞突起附着于血管壁上；脊髓损伤后0h损伤区血管连续性中断，未见GFAP免疫反应阳性细胞；72h时损伤区出现血管；1周时损伤区内血管数目较多，可见GFAP免疫反应阳性细胞；2周时损伤区空洞形成，周围可见少量GFAP免疫反应阳性细胞附着于血管；4周时损伤区内围绕空洞的血管交错排列，与GFAP免疫反应阳性细胞突起形成广泛关联。结论脊髓损伤后72h内推测是治疗脊髓损伤后损伤区组织缺血的有效时间窗，损伤后星形胶质细胞参与了血管结构的恢复。     

大鼠坐骨神经切断后腰脊髓腹角内胶质细胞和神经元的可塑性变化

目的：探讨大鼠单侧坐骨神经切断后腰脊髓腹角胶质细胞和运动神经元的反应及其相互关系。方法：用免疫组织化学技术、HE染色和Tunnel法，观察坐骨神经切断后1，6，12，24h及3，7和14d腰脊髓腹角胶质原纤维酸性蛋白(GFAP)标记的星形胶质细胞、OX-42标记的小胶质细胞及运动神经元的变化。结果：坐骨神经切断侧腰脊髓腹角可见星形胶质细胞和小胶质细胞活化，星形胶质细胞的活化早于小胶质细胞；后期运动神经元发生凋亡，HE染色显示凋亡细胞周围为反应性OX-42阳性小胶质细胞和GFAP阳性星形胶质细胞包绕。结论：研究结果提示，坐骨神经切断后切断侧腰脊髓腹角活化的胶质细胞与凋亡的运动神经元之间关系密切。     

脊髓损伤过程中β-1,4半乳糖基转移酶的表达研究

目的 探讨β-1,4半乳糖基转移酶(β-1,4-GalT)在横断性脊髓损伤后的时空表达变化以及细胞定位情况.方法 将42只成年SD大鼠随机分为假手术组和T9横断伤8 h、1 d、3 d、5 d、7 d、14 d组,每组6只.采用实时定量PCR测定损伤后各时间段β-1,4-GalT在脊髓中的表达变化;采用原位杂交与免疫荧光标记方法检测β-1,4-GalT在脊髓中的分布以及伤后的定位改变.结果 脊髓横断损伤后,β-1,4-GalT-Ⅴ在损伤上、下段表达高峰分别出现在损伤后8 h和1 d,之后逐渐下降,至伤后14 d降低至假手术组水平.增高的mRNA主要分布于损伤周围的细胞中及脊髓后角浅层的感觉神经元中.荧光原位杂交结果显示,β-1,4-GalT-Ⅴ主要分布于巨噬细胞和小胶质细胞以及病理状态下的少突胶质细胞.同时β-1,4-GalT-Ⅴ mRNA在损伤后大量表达于富含P物质和IB-4的脊髓后角浅层的感觉神经元中.结论 脊髓损伤后β-1,4-GalT在基因和细胞水平呈现明显的时空变化,并且与巨噬细胞和小胶质细胞以及病理状态下的少突胶质细胞存在共定位.该酶可能参与了损伤后的继发性损伤,即伤后早期的炎性反应,并可能与脊髓损伤后的神经病理性疼痛有关.     

间歇性θ爆发式磁刺激对高血压大鼠胼胝体髓鞘及局部炎症反应的影响

目的探究间歇性θ爆发式磁刺激对慢性高血压大鼠胼胝体区域髓鞘脱失、星形胶质细胞增生和小胶质细胞活化的改善作用。方法对雄性Sprague-Dawley大鼠随机进行双肾双夹术,制作易卒中型肾血管性高血压大鼠模型。术后22周,模型制备成功的高血压大鼠随机接受连续14 d间歇性θ爆发式磁刺激治疗(intermittent theta burst stimulation,iTBS)(高血压iTBS组,n=6)或假性刺激(高血压假刺激组,n=6),假手术大鼠接受假性刺激(假手术假刺激组,n=6)。HE染色观察胼胝体小动脉形态。免疫荧光染色观察胼胝体MBP标记的髓鞘脱失情况。免疫荧光染色观察GFAP标记的星形胶质细胞数量和IBa-1标记的小胶质细胞数量和形态,以评价星形胶质细胞增生和小胶质细胞活化。结果高血压iTBS组和高血压假刺激组出现明显小动脉管壁增厚。与假手术假刺激组相比,高血压假刺激组胼胝体MBP阳性面积比例减少(P<0.01),GFAP阳性细胞和IBa-1阳性细胞数量明显增加(P<0.01),IBa-1阳性细胞胞体增大,突起变粗,分枝变少。iTBS治疗明显增加了高血压大鼠胼胝体MBP阳性面积比例,降低GFAP阳性细胞和IBa-1阳性细胞数量(P<0.01),IBa-1阳性细胞胞体变小,突起变细,分枝变多。结论iTBS治疗可减轻高血压大鼠胼胝体区域髓鞘脱失,抑制星形胶质细胞增生和小胶质细胞活化。     

血管性认知障碍小鼠脑内少突胶质细胞再生分化障碍特点研究

目的 观察血管性认知障碍小鼠模型中,缺血性炎性损伤对室管膜下区及海马齿状回少突胶质细胞 再生分化的影响,为血管性认知障碍的缺血性炎症机制提出新的损伤途径。 方法 成年雄性CD1小鼠随机分为模型组和假手术组,每组24只,模型组采用双侧颈动脉反复缺 血再灌注法制备血管性认知障碍小鼠模型。造模后4～6 d连续腹腔注射5 -溴脱氧尿嘧啶核苷 （bromodeoxyuridine,BrdU）（150 mg/kg）标记新生细胞,分别于术后14 d和28 d每组随机取一半小鼠脑 组织进行脑切片免疫组化、免疫荧光双标共聚焦检测,标记脑组织室管膜下区和海马区的少突胶质 细胞、星形胶质细胞及神经元,观察新生少突胶质细胞增殖及分化情况,并观察星形胶质细胞的增 生活化情况。 结果 造模后14 d和28 d室管膜下区新生细胞（BrdU阳性细胞）在模型组较假手术组明显增加（P均 ＜0.001),造模28 d模型组新生神经元（BrdU/NeuN阳性细胞）较假手术组显著增加（P＜0.001)。与假 手术组相比较,术后28 d模型组海马齿状回少突胶质细胞祖细胞显著增多（P＜0.001）;少突胶质细 胞前体细胞显著减少（P =0.006）。造模后28 d模型组海马齿状回新生星形胶质细胞（BrdU/GFAP阳性 细胞）较假手术组显著增加（P =0.015）。 结论 血管性认知障碍小鼠内源性新生细胞增殖区室管膜下区与海马齿状回区均存在新生细胞反 应性增生的情况。新生细胞区分化的主要细胞为星形胶质细胞,而少突胶质细胞分化障碍,可能是血 管性认知障碍患者影像学常见皮层下白质病变的重要原因。     

MAPK/ERK信号通路在大鼠视神经损伤后小胶质细胞活化中的作用及机制研究

目的 探讨丝裂原激活蛋白激酶(MAPK)/细胞外信号调节蛋白激酶(ERK)信号通路在大鼠视神经损伤后小胶质细胞活化中的作用及机制。方法 将100只成年雄性大鼠随机分为实验组50只和对照组50只,实验组采用荧光金双侧上丘逆行标记视网膜神经节细胞并在培养7d后制作视神经损伤模型,免疫组织化学方法检测2组视网膜铺片小胶质细胞计数情况,应用蛋白免疫印记法检测2组MAPK通路的ERK蛋白表达水平及磷酸化蛋白水平,并应用免疫组化法检测2组视网膜白介素10(IL-10)和肿瘤坏死因子(TNF-α)等表达水平; 向实验组视网膜铺片添加ERK1/2通路阻断剂PD98059,再次检测其IL-10和TNF-α等表达水平及小胶质细胞计数情况。结果 与对照组比较,实验组ERK蛋白表达水平及磷酸化蛋白水平降低,视网膜铺片小胶质细胞计数降低,IL-10阳性率和TNF-α阳性率升高(P<0.05)。与阻断前比较,实验组阻断后6 h的IL-10和TNF-α等表达水平升高,小胶质细胞计数降低(P<0.05)。结论 MAPK/ERK信号通路在大鼠视神经损伤后小胶质细胞活化中具有保护作用,其机制可能通过抑制炎症因子IL-10和TNF-α等表达而减少其视神经损伤并促进小胶质细胞活化。     

溶血磷脂酸通过ERK1/2通道诱导在体海马星形胶质细胞增殖

目的:探讨溶血磷脂酸( lysophosphatidic acid,LPA)对在体海马星形胶质细胞（astrocyte,AST）活化增殖的影响及其可能的作用机制。方法:在立体定向仪下向大鼠海马CA1区注射50μmol LPA以及LPA和U0126 混合液5μl,在不同时间点采用免疫荧光双标记法检测磷酸化ERK1/2 (p-ERK1/2)和胶原纤维酸性蛋白(GFAP)含量并使用激光共聚焦扫描、三维重建观察二者空间关系。结果:LPA注射后,GFAP阳性细胞数以及p-ERK1/2显著增加(P＜0.05);p-ERK1/2早期(≤7d)主要在神经元分布区域检测到,后期(≥7d)发现p-ERK1/2主要在GFAP阳性细胞中表达。注射U0126与LPA混合液的部位未能检测到p-ERK1/2,GFAP阳性细胞数目轻度增加。结论:LPA可以通过磷酸化ERK1/2诱导大鼠海马AST增殖。     

人脐带间充质干细胞移植对大鼠脊髓损伤神经功能恢复的评价

目的 观察人脐带间充质干细胞（human umbilical cordmesenchymal stem cell，hUCMSC）移植对大鼠脊髓损伤神经功能恢复的影响。方法 SD大鼠70只，随机分为3组：脊髓半切＋hUCMSC组（n=30）、脊髓半切＋PBS组（n=30）和假手术组（n=10）。脊髓半切＋hUCMSC组和PBS组又分为头侧注射、尾侧注射和头尾两侧注射三个亚组。移植后1、7、14、21、28d观察大鼠神经功能恢复情况，应用免疫组化检测移植到脊髓的hUCMSC胶质纤维酸性蛋白（GFAP）和神经元特异性烯醇化酶（NSE）表达情况。结果 大鼠脊髓半切损害后，hUCMSC组动物较PBS组有明显的神经功能恢复。植入后28d在宿主脊髓中存活的hUCMSC细胞MABl281（mouse antiuman nuclei monoclonal antibody）染色阳性，免疫组化双标染色显示MABl28l阳性细胞亦分别有NSE或GFAP表达并向损伤部位迁移，hUCMSC来源的GFAP阳性细胞可见明显的树突生长。结论 hUCMSC移植到宿主损伤脊髓后可以存活、向损伤部位迁移，并向神经元样和星形胶质细胞分化，且可促进大鼠脊髓损伤后神经功能恢复。hUCMSC作为一种来源广泛的干细胞用于治疗脊髓损伤可能具有重要的价值。     

Expression and localization of absent in melanoma 2 in the injured spinal cord

In traumatic brain injury, absent in melanoma 2(AIM2) has been demonstrated to be involved in pyroptotic neuronal cell death. Although the pathophysiological mechanism of spinal cord injury is similar to that of brain injury, the expression and cellular localization of AIM2 after spinal cord injury is still not very clear. In the present study, we used a rat model of T9 spinal cord contusive injury, produced using the weight drop method. The rats were randomly divided into 1-hour, 6-hour, 1-day, 3-day and 6-day(post-injury time points) groups. Sham-operated rats only received laminectomy at T9 without contusive injury. Western blot assay revealed that the expression levels of AIM2 were not significantly different among the 1-hour, 6-hour and 1-day groups. The expression levels of AIM2 were markedly higher in the 1-hour, 6-hour and 1-day groups compared with the sham, 3-day and 7-day groups. Double immunofluorescence staining demonstrated that AIM2 was expressed by NeuN+(neurons), GFAP+(astrocytes), CNPase+(oligodendrocytes) and CD11 b+(microglia) cells in the sham-operated spinal cord. In rats with spinal cord injury, AIM2 was also found in CD45+(leukocytes) and CD68+(activated microglia/macrophages) cells in the spinal cord at all time points. These findings indicate that AIM2 is mainly expressed in neurons, astrocytes, microglia and oligodendrocytes in the normal spinal cord, and that after spinal cord injury, its expression increases because of the infiltration of leukocytes and the activation of astrocytes and microglia/macrophages.     

大鼠脊髓损伤后Nogo-A表达变化的免疫组织化学研究

目的观察大鼠脊髓损伤后不同时间点Nogo—A蛋白在脊髓的表达变化。方法大鼠分脊髓损伤组、假手术组和正常对照组。损伤动物存活1d、3d、7d后，分别进行Nogo—A抗体的免疫组织化学染色。结果损伤部位的灰质神经元和白质少突胶质细胞均呈明显的Nogo—A免疫阳性反应，随着损伤后存活时间的延长，两者的阳性反应细胞相对染色强度及数量均逐渐下降。结论脊髓损伤后，Nogo—A在灰质神经元有表达，其表达相对强度和表达细胞数量先明显增加，随后逐渐减少，与少突胶质细胞的表达变化相似。     

Spinal cord injury induces upregulation of Beclin 1 and promotes autophagic cell death

Autophagy is a degradation of the cytoplasm and it induces autophagic cell death in several neurodegenerative conditions. Beclin 1, a Bcl-2-interacting protein, is known to be a promoter of autophagy. We investigated the alterations in the Beclin 1 protein expression and the involvement of autophagy and autophagic cell death after spinal cord injury using a spinal cord hemisection model in mice. In the present study, the Beclin 1 expression dramatically increased at the lesion site after hemisection. The increased expression of Beclin 1 started from 4 h, peaked at 3 d, and lasted for at least 21 d after hemisection. The Beclin 1 expression was observed in neurons, astrocytes, and oligodendrocytes. The nuclei in the Beclin 1 expressing cells were round, which should normally be observed in autophagic cell death, and they were not either shrunken or fragmented as is observed in apoptotic nuclei. The results of the present study suggested that autophagy is activated in the injured spinal cord. Furthermore, autophagic cell death is considered to clearly contribute to neural tissue damage after spinal cord injury.     

The Effects of Mitotic Inhibition on the Spinal Cord Response to the Superimposed Injuries of Spinal Cord Hemisection and Peripheral Axotomy

The present study was carried out to test the hypothesis that dividing microglia are responsible for the depression of crossed phrenic nerve activity documented at 2 weeks postphrenicotomy in an injury model which superimposes the effects of spinal cord injury on peripheral axotomy. Crossed phenic nerve activity is defined as the respiratory activity recorded from the phrenic nerve during the crossed phrenic phenomenon (CPP) which is a respiratory reflex induced by respiratory stress following an ispsilateral spinal cord hemisection. Young adult female Sprague-Dawley rats were subjected to left intrathoracic phrenicotomies. Cytarabine (Cyt-A, a powerful antimitotic drug) or saline-filled miniosmotic pumps were then implanted into the cisterna magna and 2 weeks were allowed to pass at which time the CPP was induced by a left C2 spinal cord hemisection and transection of the contralateral phrenic nerve. Control studies including bromodeoxyuridine labeling of mitotic cells and a triple immunofluorescent protocol were carried out to verify that microglial cells were the primary cell type undergoing mitosis in the current injury model and that Cyt-A completely inhibited cellular proliferation. Quantitative electrophysiological analysis of crossed phrenic nerve activity showed that there is a statistically significant depression of activity at 2 weeks postphrenicotomy when animals were infused with saline compared to controls. Crossed phrenic nerve activity levels were not significantly different, however, from control levels when 2-week postphrenicotomized rats were infused with Cyt-A. Immunofluorescent studies showed that the majority of cells dividing in response to phrenicotomy were microglia. Furthermore, there were no astrocytes seen dividing at any time. From the results, we conclude that activated microglial cells may be responsible for the depression in crossed phrenic activity normally seen 2 weeks postphrenicotomy. Further, the activation of microglia may be related to the astrocytic response to injury. The activated microglial cell may be acting as a coordinator of various aspects of the injury response. Alternatively, the activation of microglia may be a necessary step in the cascade of multiple events that take place in the spinal cord after injury.     

Cell proliferation and replacement following contusive spinal cord injury

After spinal cord injury (SCI), about 50% of the oligodendrocytes and astrocytes in the residual white matter at the injury site are lost by 24 h. However, chronically after SCI, the density of oligodendrocytes is normal. Previous studies have shown that the adult rat spinal cord contains a pool of proliferating glial progenitors whose progeny could help restore cell density after injury. To study proliferation in response to injury, we performed SCI on adult female rats at the T8 level, using a standardized contusion model. Animals received bromodeoxyuridine (BrdU) injections during the first week after SCI, and were perfused within 2 h for acute studies, and at 6 weeks for chronic studies. The tissue was analyzed using immunohistochemical detection of BrdU and cell marker antigens. We demonstrate that cell proliferation in the residual white matter is increased at 1-7 days after SCI, peaking on day 3. Dividing cells include oligodendrocytes, astrocytes, microglia/macrophages, and a high proportion of NG2(+) glial precursors. By 6 weeks, some cells that had been labeled 2-4 days after SCI were still present. Double immunohistochemistry showed that while very few of these cells expressed NG2 or the microglia/macrophage marker OX42, about 50% expressed CC1 or glial fibrillary acidic protein (GFAP), markers of mature oligodendrocytes and astrocytes, respectively. The post-injury environment represented by residual white matter is thus permissive to the differentiation of glial precursors. Cells that are stimulated to divide during the first week after SCI develop chronically into mature phenotypes that replace macroglia lost after injury.     

Rat hair follicle stem cells differentiate and promote recovery following spinal cord injury

Emerging studies of treating spinal cord injury （SCI） with adult stem cells led us to evaluate the effects of transplantation of hair follicle stem cells in rats with a compression-induced spinal cord lesion. Here, we proposed a hypothesis that rat hair follicle stem cell transplantation can promote the recovery of injured spinal cord. Compression-induced spinal cord injury was induced in Wistar rats in this study. The bulge area of the rat vibdssa follicles was isolated, cultivated and characterized with nestin as a stem cell marker. 5-Bromo-2＇-deoxyuridine （BrdU） labeled bulge stem cells were transplanted into rats with spinal cord injury. Immunohistochemical staining results showed that some of the grafted cells could survive and differentiate into oligodendrocytes （receptor-interacting protein positive cells） and neuronal-like cells （~lll-tubulin positive cells） at 3 weeks after transplantation. In addition, recovery of hind limb locomotor function in spinal cord injury rats at 8 weeks following cell transplantation was assessed using the Basso, Beattie and Bresnahan （BBB） locomotor rating scale. The results demon- strate that the grafted hair follicle stem cells can survive for a long time period in vivo and differentiate into neuronal- and glial-like cells. These results suggest that hair follicle stem cells can promote the recovery of spinal cord injury.     

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 grou     

大鼠脊髓半横断损伤后凋亡相关基因的表达变化

目的探讨脊髓半横断损伤后凋亡相关基因Bc l-2、Bax、Fas在蛋白水平的表达变化规律及神经细胞凋亡的分子生物学机制。方法在成年SD大鼠脊髓T9~T10间半横断,取损伤位点尾侧段T10节段制作冰冻切片,运用Bc l-2、Bax、Fas兔抗血清以免疫组化亲合素-生物素-过氧化物酶复合物法(ABC)法染色。观察并计数腹角Bc l-2、Bax、Fas的阳性神经元数。结果Bc l-2、Bax、Fas主要分布于正常大鼠脊髓腹角神经元细胞浆,损伤后腹角Bc l-2、Bax、Fas阳性神经元数在3 d组(n=6)、7 d组(n=6)、21 d组(n=6)均较假手术组(n=6)明显增加(P<0.01),Bax、Fas阳性神经元数在术后3d时达高峰,随伤后时间的延长进行性减少(P<0.05)。Bc l-2阳性神经元数在术后7 d时达高峰,3 d组与21 d组比较没有显著差异。结论脊髓半横断损伤(hSC I)后,由Fas抗原参与的死亡受体途径及Bc l-2、Bax参与的线粒体途径均参与了hSC I后细胞的凋亡过程。     

他克莫司促进神经干细胞移植大鼠脊髓损伤的再生与修复

背景：研究证实,他克莫司不仅抑制T细胞的增殖、活化,还能抑制小胶质细胞、巨噬细胞等炎症细胞在损伤局部聚集、活化及相关炎症因子的释放,减轻继发性炎症反应对原发损伤周围正常组织的破坏,从而对损伤局部的神经组织起保护作用。 目的：观察他克莫司对神经干细胞移植大鼠脊髓损伤后再生修复的影响。 方法：分离培养孕13d SD大鼠神经干细胞。显微镜下动脉瘤夹夹闭SD大鼠T8脊髓,建立压迫型脊髓损伤动物模型。损伤后7 d随机数字表分为3组：对照组,于损伤中心定向注射生理盐水;细胞移植组,于损伤中心定向注射神经干细胞;他克莫司组,于损伤中心定向注射神经干细胞同时给予免疫抑制剂他克莫司1 mg/(kg•d)腹腔注射连续7 d。1,2,4,8周后,通过BDA顺行示踪、苏木精-伊红与免疫组化染色及电镜检测,观察移植后脊髓组织再生和神经元的变化。 结果与结论：对照组在损伤中心端远侧无神经纤维通过。细胞移植组与他克莫司组在治疗1周后有部分神经纤维通过,8周均有部分BDA阳性标记的皮质脊髓束再生通过脊髓损伤部位,特别是他克莫司组可延续至距损伤中心1.7 cm 。苏木精-伊红染色显示,细胞移植组与他克莫司组2周时坏死灶开始缩小,泡沫细胞减少。电镜结果显示,他克莫司组1周时即出现较正常的微丝和微管结构,8周时星形细胞、许旺细胞、髓鞘典型多见,神经轴突的终末有较多的兴奋性递质和不典型的轴树连接,出现较多的结构正常的髓鞘。说明损伤大鼠移植神经干细胞后联合应用他克莫司后可减轻早期的急性炎症反应,保证神经细胞的存活,具有神经保护和神经营养作用,可加快神经功能的恢复。