VEGF表达对大鼠坐骨神经嵌压性损害的神经保护作用

目的 探讨血管内皮细胞生长因子（VEGF）的表达对周围神经嵌压症病理损伤和神经功能损害的保护作用。方法 将80只SD大鼠按体重随机分层分组制作坐骨神经嵌压性损害的动物模型，取嵌压后第12小时、72小时、7天与第4周的大鼠坐骨神经，分别采用免疫组化与病理学、电生理学的方法检测VEGF水平与病理变化、神经传导速度、脊髓神经元计数等，并将各项检测结果进行对比，运用正常对照组、模型组、前列地尔组和盐酸丁咯地尔组采用SAS统计软件9．1．3进行方差分析统计处理。结果 （1）嵌压大鼠坐骨神经后，除正常对照组外12h起各组背根神经节细胞VEGF表达开始增加，72h达到高峰后开始下降，一周时接近正常水平。正常对照组只轻度表达。与正常对照组比较，其余各组各时段背根神经节细胞VEGF表达水平均显著增加（P〈0．05），前列地尔组和盐酸丁咯地尔组较模型组为优（P〈0．05）、表达的数量增加、持续时间延长。（2）嵌压大鼠坐骨神经4周后，正常对照组正常，其余各组病理变化、脊髓神经元计数均明显较正常对照组差（P〈0．01）；而前列地尔组和盐酸丁咯地尔组第4周时上述诸项结果虽较正常对照组差（P〈0．05），但均较模型组为优（P〈0．05）。（3）嵌压大鼠坐骨神经4周时，正常对照组正常，其余各组大鼠坐骨神经传导速度均明显较正常对照组差（P〈0．01）；而前列地尔组和盐酸丁咯地尔组第4周时上述诸项结果虽较正常对照组差（P〈0．05），但均较模型组为优（P〈0．05）。（4）VEGF表达增加组之病理改变减轻、神经功能恢复增加。结论对于周围神经嵌压性损害，VEGF表达的增加可减轻周围神经病理损害、提高神经传导速度、促进周围神经损伤的修复。     

周围神经电刺激促进相应脊髓节段及背根神经节表达pCREB和BDNF

目的研究电刺激促进神经再生的机理,为周围神经电刺激促进脊髓损伤修复治疗策略的建立提供实验依据。方法将切断坐骨神经的雄性SD大鼠24只随机分为对照组(不实施电刺激)和实验组(实施电刺激),每组12只。采用免疫组化技术(荧光法),检测相应脊髓节段及背根神经节中磷酸化环磷酸腺苷反应原件结合蛋白(p CREB)的表达,并对脊髓及背根神经节中阳性神经元进行计数。采用实时定量聚合酶链反应(RT-q PCR)对脑源性神经营养因子(BDNF)mRNA水平进行测定。结果经免疫组化染色发现,术后第3 d实验组脊髓和背根神经节p CREB阳性神经元数大于对照组(P0.05),且经RT-q PCR分析,术后第3 d实验组脊髓及背根神经节BDNF mRNA水平较对照组明显升高(P0.05)。结论电刺激作用于周围神经损伤近端,可上调相应脊髓节段及背根神经节神经元内p CREB和BDNF的表达水平。     

综合足部护理对糖尿病周围神经病变患者的临床作用

目的评价综合足部护理对糖尿病周围神经病变患者的临床作用。方法将2008-02—2011-07我院收治的糖尿病周围神经病变患者144例随机分为观察组72例和对照组72例,对照组采用常规治疗,控制血糖;观察组在常规治疗基础上配合综合足部护理,检测治疗前和治疗3个月后患者的双侧正中神经、腓神经、尺神经和胫后神经的周围神经传导速度,观察患者双下肢症状的改善情况,评价2组空腹和餐后2h血糖下降情况。结果观察组总有效率91.7%,高于对照组的83.3%,2组比较差异有统计学意义(χ2=5.16,P<0.05);2组治疗前周围神经传导速度比较差异无统计学意义(P>0.05),治疗后周围神经传导速度均有所改善,观察组治疗前后双侧正中神经、腓神经、尺神经和胫后神经的周围神经传导速度差异均有统计学意义(P<0.05),对照组仅胫后神经的周围神经传导速度差异有统计学意义(P<0.05),观察组改善效果明显优于对照组(P<0.05);观察组空腹血糖和餐后2h血糖下降较对照组明显,2组比较差异有统计学意义(P<0.05)。结论综合足部护理可以改善周围神经的传导速度,有利于糖尿病周围神经病变的恢复,提高治疗效果,对治疗糖尿病周围神经病变有重要意义。     

维生素B12与丁咯地尔治疗糖尿病周围神经病变临床观察

目的 观察维生素B12、丁咯地尔对糖尿病周围神经病变患者症状缓解和神经传导速度的影响.方法 116例周围神经病变患者分为治疗组和对照组,分别给予维生素B12、丁咯地尔和前列腺素E1静滴,给药前及给药2周后观察症状缓解情况和四肢神经传导速度. 结果 给药2周后,对照组各神经传导速度均明显增快(P<0.01),治疗组各神经传导速度亦增快(P<0.01),治疗组与对照组比较差异无统计学意义(P>0.05).治疗组总有效率为80.0%,对照组为89.3%,2组比较差异无统计学意义(P>0.05).结论 维生素B12、丁咯地尔治疗糖尿病周围神经病变具有较好的安全性和有效性.     

TBOA抑制谷氨酸转运体功能对全脑缺血性癫癎的影响

目的 观察新型的谷氨酸转运体抑制剂TBOA对全脑缺血性癫癎的发生及神经病理的作用,探索全脑缺血性癫癎的治疗新方法.方法 应用稳定可靠的大鼠胸部压迫8 min全脑缺血性癫癎模型,分为缺血癫癎组和TBOA治疗组.胸部挤压前3 d大鼠侧脑室内注射TBOA,研究两组癫癎的发生率、海马及皮质病理改变、神经元计数.结果 缺血后24 h癫癎发生率在缺血癫癎组为61%,TBOA治疗组为40%,光镜病理显示,TBOA治疗组损害程度轻于缺血癫癎组.海马CAI区神经元计数缺血早期(24 h,72 h组),缺血癫癎组与TBOA治疗组比较无显著性差异,P＞0.05;缺血后期(5 d,7 d组),缺血癫癎组神经元计数少于TBOA治疗组,P均＜0.05.皮质区变化规律同海马CAI区.结论 全脑缺血前应用谷氨酸转运体抑制剂TBOA能降低癫癎的发生率,并改善缺血后神经病理损害.     

外源性血管内皮生长因子对大鼠损伤脊髓神经元的作用

目的研究外源性血管内皮生长因子(VEGF)局部应用对大鼠脊髓损伤(SCI)后脊髓灰质神经元的作用。方法采用改良Allen氏重量打击法建立大鼠急性SCI模型,将72只模型大鼠随机分为VEGF治疗组〔人工基底膜(Matrigel蛋白胶)10μL+重组人VEGF1650.2μg〕、基底膜对照组(Matrigel蛋白胶10μL)和空白对照组(生理盐水10μL)3组,分别经蛛网膜下腔给药。于SCI后1、2、3、4周分别观察模型鼠脊髓横切面灰质神经元数量、神经元截面积和尼氏体密度恢复情况。结果 SCI后1~4周VEGF治疗组脊髓横切面灰质神经元数量(分别为76.34±6.25、108.25±11.74、144.33±13.22、165.96±18.11)和神经元截面积〔分别为(177.87±14.42)(、229.63±21.74)(、340.55±32.66)(、390.30±46.19)μm2〕均高于同期基底膜对照组〔神经元数量分别为40.89±7.20、50.61±13.11、59.78±9.46、80.13±10.84,神经元截面积分别为(108.98±15.03)(、148.53±18.38)、(163.22±16.77)(、208.87±29.58)μm2〕和空白对照组〔神经元数量分别为37.66±6.69、52.36±5.17、60.58±9.13、78.56±13.56,神经元截面积分别为(114.55±14.22)(、139.24±15.17)、(157.11±20.26)(、185.23±21.65)μm2〕(P<0.01,P<0.05)。SCI后1周时VEGF治疗组神经元尼氏体密度(0.2089±0.0210)与基底膜对照组(0.2012±0.0145)、空白对照组(0.1982±0.0106)比较差异均无统计学意义(P>0.05),SCI后2、3、4周,VEGF治疗组尼氏体密度(分别为0.2489±0.0217、0.2908±0.0327、0.3508±0.0362)亦大于基底膜对照组(分别为0.2198±0.0214、0.2406±0.0198、0.2605±0.0322)和空白对照组(分别为0.2044±0.0231、0.2356±0.0311、0.2582±0.0245)(均P<0.05)。两对照组各指标均无统计学差异。结论局部应用外源性VEGF可能对SCI后大鼠脊髓灰质神经元具有保护作用。     

甲钴胺联合前列地尔治疗46例糖尿病周围神经病变的疗效观察

目的探讨甲钴胺联合前列地尔治疗糖尿病周围神经病变的临床疗效和安全性。方法采用随机数字表法将91例糖尿病周围神经病变患者分为2组,对照组单用甲钴胺注射液肌内注射,治疗组给予甲钴胺联合前列地尔治疗,连续治疗30d,观察2组患者的临床疗效和药物安全性。结果治疗组周围神经传导速度明显高于对照组,P<0.01;治疗组总有效率95.65%,优于对照组的80.00%,P<0.05;组间药物不良反应比较,P>0.05。结论甲钴胺联合前列地尔治疗糖尿病周围神经病变疗效确切,能够有效改善周围神经血流供应和促进神经功能修复,药物不良反应发生率低,值得临床推广应用。     

周围神经减压改善DPN大鼠神经微循环、促进神经修复的作用机制

目的从细胞生物学、分子生物学水平证实神经双重卡压加剧糖尿病周围神经病变(DPN)神经损伤,探讨周围神经减压术延缓或修复神经损伤的作用机制。方法构建Mackinnon DPN大鼠模型;苏木精-伊红染色测定卡压远端神经微循环血管形态、分布状况。透射电镜观察卡压远端神经微循环血管结构状况以及施旺细胞形态变化和分布密度。免疫组织化学染色测定神经末梢NGF、TrkA、GAP-43含量,用以评价神经修复功能。结果 DPN组大鼠神经微血管分布密度明显减少,施旺细胞分布密度明显降低(P0.05),施旺细胞及血管内皮细胞呈现典型的凋亡形态改变,NGF、Tr KA、GAP-43含量也明显减少(P0.05);DPN减压组神经微血管分布密度有所改善,施旺细胞分布密度明显提高(P0.05),NGF、Tr KA、GAP-43含量明显提高(P0.05)。结论 DPN大鼠神经卡压后导致微循环障碍,引发施旺细胞数量减少,影响受损神经的自我修复功能;周围神经减压术可以有效缓解或逆转这一病理变化。     

神经妥乐平联合前列地尔治疗糖尿病周围神经病临床研究

目的探讨神经妥乐平联合前列地尔治疗糖尿病周围神经病变的疗效。方法对74例糖尿病周围神经病患者分治疗组38例和照组36例。2组入院后均1次/d静滴前列地尔针20μg,治疗组1次/d静滴神经妥乐平针剂7.2 U,共3周。观察2组的观察治疗前后临床症状及神经传导速度。结果给予神经妥乐平联合前列地尔治疗组临床症状(总有效率89.5%,P<0.05)、神经传导速度改善明显好于单用前列地尔(P<0.01)。结论神经妥乐平联合前列地尔治疗可以有效改善临床症状及神经传导速度进而改善预后。     

糖尿病患者周围神经传导速度的研究

目的:通过周围神经传导速度(NCV)的研究,早期诊断糖尿病(DM)患者的糖尿病性周围神经病变。方法:应用上海海军医学研究所NDI-200F神经电检诊仪,对DM组95例患者行尺神经、正中神经、胫神经和腓神经运动传导速度(MCV)及尺神经、正中神经、腓肠神经感觉传导速度(SCV)检测与30例健康人组对照。结果:DM组95例, NCV异常率为77.89%(74/95)。共检测665条神经,MCV380条,异常率55.26%,SCV285条,异常率50.88%,差异无显著性意义(P>0.05)。上肢检测380条神经,异常率45.53%,下肢检测285条神经,异常率63.86%,差异有显著性意义(P<0.05)。DM组SCV波幅减低率为53.66%。DM组按病程分为三组,<5年,30例,异常率28.10%;≥5年,31 例,异常率为54.84%;≥10年,34例,异常率74.37%,组间差异均有非常显著性意义(P<0.01)。DM组中29例无周围神经病变症状与体征,NCV异常11例(37.93%)。结论:周围神经传导速度检测不但可以早期诊断糖尿病患者的糖尿病性周围神经病变,而且此方法可靠、简便、无创。     

钙通道阻滞剂对大鼠坐骨神经损伤后c-fos表达及神经功能的影响

目的探讨钙通道阻滞剂(CCB)对周围神经损伤后c-fos表达及神经功能的影响。方法制作坐骨神经嵌压性损伤大鼠模型,给予模型大鼠分别腹腔注射氟桂利嗪1mg/kg(低剂量组)、2mg/kg(高剂量组),或生理盐水10ml/kg(模型组)。在坐骨神经嵌压后第1周、第4周时取大鼠坐骨神经,采用免疫组织化学、行为医学和电生理学的方法测定c-fos阳性细胞数及第4周时足趾间距、神经传导速度(NCV);并与正常大鼠比较。结果(1)损伤后1周时,模型组、氟桂利嗪低剂量组坐骨神经c-fos阳性细胞数显著多于正常对照组(均P<0.01);氟桂利嗪高剂量组c-fos阳性细胞数轻度增加,也显著多于正常对照组(P<0.05),但明显少于模型组和氟桂利嗪低剂量组(均P<0.01);损伤4周时各组c-fos阳性细胞数均无明显增高。(2)损伤后4周时,模型组和氟桂利嗪低剂量组、高剂量组坐骨神经NCV显著慢于正常对照组(均P<0.01),氟桂利嗪低剂量组、高剂量组的NCV快于模型组(P<0.05,P<0.01)。(3)损伤后4周时,模型组大鼠右后肢足趾间距明显小于其他3组(均P<0.01);氟桂利嗪高剂量组、低剂量组与正常对照组比较差异无统计学意义(均P>0.05)。结论CCB使周围神经损伤后早期c-fos表达下调,并使神经功能受损减轻。     

Preemptive analgesic effects of low-dose ketamine on growth-associated protein expression in dorsal root ganglion of chronic constriction injury model rats★

BACKGROUND： Ketamine is a noncompetitive N-methyl-D-aspartate （NMDA） receptor antagonists and plays an important role in the treatment of pain. OBJECTIVE： To analyze the preemptive analgesic effects of different doses of ketamine on growth-associated protein-43 （GAP43） expression in dorsal root ganglion in a rat model of chronic sciatic nerve constricted injury, and to study the differences between high-dose and low-dose ketamine DESIGN： Randomized controlled animal study. SETTING： Medical College of Shantou University. MATERIALS： Thirty-five adult male Sprague Dawley rats were provided by the Experimental Animal Center of Guangzhou University of Traditional Chinese Medicine. Ketamine hydrochloride injection was provided by Hengrui Pharmaceutical Co., Ltd., Jiangsu. METHODS： This study was performed at the Immunological Laboratory, Medical College of Shantou University from September to December 2006. Model of chronic sciatic nerve constricted injury： after anesthesia, the right sciatic nerve was exposed and ligated l-cm distal to the ischiadic tuberosity with a No. 3-0 cat gut suture. Grouping and intervention： 35 rats were randomly divided into 4 groups： normal control group （n = 5）, chronic constriction injury （CCI） group （n = 10）, low-dose ketamine group （n = 10）, and high-dose ketamine group （n = 10）. Rats in the normal control group did not undergo any surgery or drug intervention. Rats in the CCI group received intraperitoneal injection of saline （1 mL）, and their sciatic nerves were ligated after 10 minutes. Rats in the low-dose ketamine group underwent intraperitoneal injection of ketamine （25 mg/kg） 10 minutes prior to ligation of sciatic nerve; while, rats in the high-dose ketamine group were given intraperitoneal injection of ketamine （50 mg/kg） 10 minutes prior to ligation of sciatic nerve. On the third and the seventh days after surgery, dorsal root ganglion were resected from the sciatic nerve and cut into sections. MAIN OUTCOME MEASURES：     

Substance P and calcitonin gene-related peptide expression in dorsal root ganglia in sciatic nerve injury rats

The neuropeptides, substance P and calcitonin gene-related peptide, have been shown to be involved in pain transmission and repair of sciatic nerve injury. A model of sciatic nerve defect was prepared by dissecting the sciatic nerve at the middle, left femur in female Sprague Dawley rats. The two ends of the nerve were encased in a silica gel tube. L5 dorsal root ganglia were harvested 7, 14 and 28 days post sciatic nerve injury for immunohistochemical staining. Results showed that substance P and cal- citonin gene-related peptide expression increased significantly in dorsal root ganglion of rats with sci- atic nerve injury. This increase peaked at 7 days, declined at 14 days, and reduced to normal levels by 28 days post injury. The findings indicate that the neuropeptides, substance P and calcitonin gene- related peptide, mainly increased in the early stages after sciatic nerve injury.     

Changes in tactile stimuli-induced behavior and c-Fos expression in the superficial dorsal horn and in parabrachial nuclei after sciatic nerve crush

Neurons in the superficial laminae of the dorsal horn are dominated by input from peripheral nociceptors. Following peripheral nerve injury, low threshold mechanoreceptive Abeta-fibers sprout from their normal termination site in laminae III/IV into laminae I-II and this structural reorganization may contribute to neuropathic tactile pain hypersensitivity. We have now investigated whether a sciatic nerve crush injury alters the behavioral response in rats to tactile stimuli and whether this is associated with a change in the pattern of c-Fos expression in the dorsal horn and the parabrachial area of the brainstem. Sciatic nerve crush resulted in a patchy but marked tactile allodynia manifesting first at 3 weeks and persisting for up to 52 weeks. C-Fos expression in the dorsal horn and parabrachial region was never observed on brushing the skin of the sciatic nerve territory in animals with intact nerves, but was found after sciatic nerve crush with peripheral regeneration. We conclude that after nerve injury, low threshold mechanoreceptor fibers may play a major role in producing pain-related behavior by activating normally nociceptive-specific regions of the central nervous system such as the superficial laminae of the dorsal horn and the parabrachial area.     

Cytokine regulation of MMP-9 in peripheral glia: implications for pathological processes and pain in injured nerve

Matrix metalloproteinase-9 (MMP-9) is an extracellular protease that is induced in Schwann cells hours after peripheral nerve injury and controls axonal degeneration and macrophage recruitment to the lesion. Here, we report a robust (90-fold) increase in MMP-9 mRNA within 24 h after rat sciatic nerve crush (1 to 60 days time-course). Using direct injection into a normal sciatic nerve, we identify the proinflammatory cytokines TNF-alpha and IL-1beta as potent regulators of MMP-9 expression (Taqman qPCR, zymography). Myelinating Schwann cells produced MMP-9 in response to cytokine injection and crush nerve injury. MMP-9 gene deletion reduced unstimulated neuropathic nociceptive behavior after one week post-crush and preserved myelin thickness by protecting myelin basic protein (MBP) from degradation, tested by Western blot and immunofluorescence. These data suggest that MMP-9 expression in peripheral nerve is controlled by key proinflammatory cytokine pathways, and that its removal protects nerve fibers from demyelination and reduces neuropathic pain after injury.     

Diminished dorsal root GABA sensitivity following chronic peripheral nerve injury

The depolarizing effect of gamma-aminobutyric acid (GABA) on rat lumbar dorsal roots was studied in a sucrose gap chamber following axotomy or crush injury of the sciatic nerve or dorsal root. The mean depolarization elicited by GABA on normal dorsal roots (3.96 +/- 0.71 mV, N = 14) was significantly reduced following chronic sciatic axotomy (2.02 +/- 0.99 mV, N = 15). Chronic sciatic crush injury had no significant effect on dorsal root GABA sensitivity. The amplitudes of the dorsal root compound action potentials were the same from rats with normal and injured sciatic nerves, indicating that axons proximal to the sciatic nerve lesion did not undergo appreciable degeneration. A marked loss of dorsal root GABA sensitivity was also seen following dorsal root axotomy or crush injury (1.02 +/- 0.98 mV (N = 10) and 0.69 +/- 0.70 mV (N = 9), respectively). These results indicate that GABA sensitivity of dorsal roots is attenuated following peripheral nerve lesions in which regeneration and functional reconnection with peripheral targets are prevented. Previous work indicates that the primary afferent depolarization is reduced under similar conditions. The reduction in GABA sensitivity of dorsal root fibers described here may have a contributory role in the reduced primary afferent depolarization that follows peripheral nerve transection, which has pathophysiologic implications in chronic pain syndromes.     

Electrical stimulation impairs early functional recovery and accentuates skeletal muscle atrophy after sciatic nerve crush injury in rats

Neuromuscular recovery after peripheral nerve lesion depends on the regeneration of severed axons that re‐establish their functional connection with the denervated muscle. The aim of this study was to determine the effects of electrical stimulation (ES) on the neuromuscular recovery after nerve crush injury in rats. Electrical stimulation was carried out on the tibialis anterior (TA) muscle after sciatic nerve crush injury in a rat model. Six ES sessions were administered every other day starting from day 3 postinjury until the end of the experiment (day 14). The sciatic functional index was calculated. Muscle excitability, neural cell adhesion molecule (N‐CAM) expression, and muscle fiber cross‐sectional area (CSA) were accessed from TA muscle. Regenerated sciatic nerves were analyzed by light and confocal microscopy. Both treated (crush+ES) and untreated (crush) groups had their muscle weight and CSA decreased compared with the normal group (P < 0.05). Electrical stimulation accentuated muscle fiber atrophy more in the crush+ES than in the crush group (P < 0.05). N‐CAM expression increased in both crush and crush+ES groups compared with the normal group (P < 0.05). Regenerated nerves revealed no difference between the crush and crush+ES groups. Nevertheless, functional recovery at day 14 post‐injury was significantly lower in crush+ES group compared with the crush group. In addition, the crush+ES group had chronaxie values significantly higher on days 7 and 13 compared with the crush group, which indicates a decrease in muscle excitability in the crush+ES animals. The results of this study do not support a benefit of the tested protocol of ES during the period of motor nerve recovery following injury. Muscle Nerve, 2010     

GAP-43 mRNA in Rat Spinal Cord and Dorsal Root Ganglia Neurons: Developmental Changes and Re-expression Following Peripheral Nerve Injury

The expression of growth-associated protein GAP-43 mRNA in spinal cord and dorsal root ganglion (DRG) neurons has been studied using an enzyme linked in situ hybridization technique in neonatal and adult rats. High levels of GAP-43 mRNA are present at birth in the majority of spinal cord neurons and in all dorsal root ganglion cells. This persists until postnatal day 7 and then declines progressively to near adult levels (with low levels of mRNA in spinal cord motor neurons and 2000–3000 DRG cells expressing high levels) at postnatal day 21. A re-expression of GAP-43 mRNA in adult rats is apparent, both in sciatic motor neurons and the majority of L4 and L5 dorsal root ganglion cells, 1 day after sciatic nerve section. High levels of the GAP-43 mRNA in the axotomized spinal motor neurons persist for at least 2 weeks but decline 5 weeks after sciatic nerve section, with the mRNA virtually undetectable after 10 weeks. The initial changes after sciatic nerve crush are similar, but by 5 weeks GAP-43 mRNA in the sciatic motor neurons has declined to control levels. In DRG cells, after both sciatic nerve section or crush, GAP-43 mRNA re-expression persists much longer than in motor neurons. There was no re-expression of GAP-43 mRNA in the dorsal horn of the spinal cord after peripheral nerve lesions. Our study demonstrates a similar developmental regulation in spinal cord and DRG neurons of GAP-43 mRNA. We show moreover that failure of re-innervation does not result in a maintenance of GAP-43 mRNA in axotomized motor neurons.     

纤维蛋白凝胶携载血管内皮生长因子对大鼠损伤坐骨神经运动功能的影响

背景：坐骨神经损伤后的修复方法多样,但由于坐骨神经解剖和功能上的特殊性,神经功能的恢复仍不理想。 目的：观察局部应用纤维蛋白凝胶携载血管内皮生长因子,对损伤坐骨神经组织神经功能恢复的疗效。 方法：将Wistar大鼠左侧坐骨神经切断,神经两断端原位缝合,制作大鼠坐骨神经损伤动物模型,然后随机分为2组,实验组于坐骨神经切断处外膜内、外注射纤维蛋白凝胶/血管内皮生长因子复合体;对照组于同处注射血管内皮生长因子165质粒。于用药后4,8,12周行大体观察、神经功能指数检测、电生理检测(测运动神经传导速度)。 结果与结论：两组动物伤口均为一期愈合。实验组用药后1周有6只出现足底溃疡伴肌萎缩;对照组有5只出现足底溃疡。实验组4周时,纤维蛋白凝胶基本被吸收;8周时完全吸收;12周时,神经外形基本正常。对照组4周时,神经轻度充血、水肿;8周时,神经无水肿,与周围组织见少量粘连;12周时,神经周围见瘢痕形成。实验组4,8周的神经功能指数、运动神经传导速度较对照组降低(P < 0.05),12周无显著性差异(P > 0.05)。提示纤维蛋白凝胶可以作为血管内皮生长因子的载体,纤维蛋白凝胶携载血管内皮生长因子给药可以促进损伤神经结构和功能的恢复。 关键词：坐骨神经;损伤;纤维蛋白凝胶;血管内皮生长因子;载体 doi:10.3969/j.issn.1673-8225.2010.29.015