人参皂苷Re对重症急性胰腺炎小鼠小肠黏膜的影响及调控机制

目的 探讨人参皂苷Re通过调控Janus激酶2/信号转导子与转录激活子3(JAK2/STAT3)通路对重症急性胰腺炎(SAP)小鼠小肠黏膜的影响及作用机制.方法 48只小鼠分为对照组、SAP组、SAP+人参皂苷Re组和SAP+人参皂苷Re+LY2784544组(n= 12).通过腹腔注射雨蛙肽溶液(禁食12 h后,10...     

人参皂苷Rb1减轻人脐静脉内皮细胞氧化损伤

目的探讨人参皂苷Rb1(gRb1)对过氧化氢(H_2O_2)致人脐静脉内皮细胞(HUVECs)氧化损伤的影响。方法将HUVECs分为对照组、H_2O_2(20、40、80和160μmol/L)组、gRb1(10、20和40μmol/L)干预组。MTT法测定细胞存活率;annexin V-FITC/PI双染法检测凋亡;黄嘌呤氧化酶法测定SOD1活性;硫代巴比妥比色法计算MDA含量;Western blot测定细胞间黏附分子-1(ICAM-1)和血管细胞黏附分子-1(VCAM-1)蛋白表达。结果与对照组相比,H_2O_2呈浓度依赖性抑制细胞存活率(P0.05),增加细胞凋亡(P0.05),抑制SOD1活性(P0.05),增加MDA含量(P0.05),促进ICAM-1和VCAM-1蛋白表达(P0.05)。gRb1干预能够显著缓解上述指标的变化。结论 gRb1通过抑制细胞凋亡、改善氧化应激水平和抑制ICAM-1及VCAM-1蛋白表达减轻HUVECs氧化损伤。     

人参皂苷Rb1对缺氧诱导N9细胞应激活化反应的影响

目的 探讨人参皂苷Rb1对缺氧诱导的小胶质细胞活化的的影响. 方法 通过人参皂苷Rb1对缺氧状态下N9细胞的干预,检测细胞形态、增殖活力改变.采用ELISA法、荧光探针DAF-FM DA、Griess Reagent法检测细胞TNF-α、O-2产量以及NO含量改变的影响.借助化学发光法、免疫荧光法分别检测各组细胞线粒体膜电位、细胞色素C含量. 结果 无论是预防性给药还是治疗性给药,人参皂苷Rb1能明显降低缺氧诱导活化的N9细胞NO、O-2以及TNF-α产量,抑制线粒体膜电位的降低,缓解细胞内细胞色素C含量的改变程度. 结论 人参皂苷Rb1均能在一定程度上下调由于缺氧活化导致神经毒性因子的高表达,稳定细胞线粒体的结构和功能,抑制缺氧诱导的N9细胞活化.     

人参皂苷Rb1对大鼠脑缺血再灌注损伤中NAIP表达的影响

目的:观察人参皂苷Rb1对神经元凋亡抑制蛋白(neuronal apoptosis inhibitory protein,NAIP)在脑缺血再灌注损伤中表达的影响,探讨人参皂苷Rb1对缺血性脑病的防治机制.方法:线栓法阻断大鼠大脑中动脉2 h,再灌注3 h～5 d制备脑缺血再灌注模型,应用免疫组织化学方法标记NAIP阳性细胞,观察人参皂苷Rb1对NAIP阳性细胞数的影响.结果:缺血再灌注后,缺血半暗带内的NAIP阳性细胞表达增加,海马CA 1区等部位的NAIP阳性细胞数量也明显增加,而缺血中心区无NAIP阳性细胞的表达.实验对照组中NAIP阳性细胞数量随再灌注时间延长逐渐升高,12 h达到高峰,至5 d时NAIP阳性细胞数量表达低于正常水平.实验用药组中NAIP阳性细胞数量在2 d时达到高峰,且其高峰值明显高于实验对照组中的高峰值,后随再灌注时间的延长而逐渐下降,至5 d时仍处于较高水平.结论:脑缺血再灌注后,NAIP表达增加是脑组织对损伤的一种保护性反应,其对缺血区周围的神经细胞的保护作用更为明显.NAIP在脑组织中的表达具有一定的时间规律性,并且人参皂苷Rb1可能通过上调NAIP的表达发挥对受损脑组织的保护作用.     

人参皂苷Rg1对大鼠胸腺结构与功能的影响

目的 探讨人参皂苷Rg1对大鼠胸腺组织结构与功能的影响及相关机制。 方法 SD大鼠随机分为2组,每组10只。Rg1注射组,腹腔注射Rg1 20mg/kg,qd×28d;对照组,等时注射等量生理盐水。药物注射完成后第2天,取胸腺称重测定胸腺指数,石蜡切片与HE染色观察胸腺组织结构;衰老相关β-半乳糖苷酶（SA-β-Gal）染色检测胸腺细胞衰老,细胞计数试剂盒（CCK-8）检测胸腺细胞对刀豆蛋白A（ConA）刺激的增殖能力,ELISA检测胸腺细胞分泌肿瘤坏死因子-α（TNF-α）、粒细胞 巨噬细胞集落刺激因子（GM-CSF）、白细胞介素（IL)-2与IL-6的能力,流式细胞术检测胸腺细胞周期、细胞凋亡率与活性氧（ROS）含量,酶学检测丙二醛（MDA）、超氧化物歧化酶（SOD）含量与还原性谷胱甘肽（GSH）与氧化性谷胱甘肽（GSSH）的比值,Western blotting 检测细胞衰老相关蛋白P21、P53、Rb表达。 结果 与对照组相比,注射Rg1能提升大鼠胸腺指数,增加胸腺皮质面积比例,提高胸腺细胞增殖能力和S期比例,降低G₁期与G₂/M期细胞比例,减少胸腺细胞凋亡和SA-β-Gal阳性细胞百分率,促进胸腺细胞分泌GM-CSF,TNF-α、IL-2、IL-6,提升胸腺细胞SOD活性和GSH/GSSG比例,降低ROS、MDA含量,下调P53、P21、RB蛋白表达。 结论 人参皂苷Rg1对大鼠胸腺结构与功能有明确的保护作用,其机制可能与抑制氧化损伤和下调p53/p21/Rb信号通路有关。     

人参皂苷Rg1和Rb1对流感病毒感染细胞的影响及其机制研究

目的 研究人参皂苷Rg1和Rb1对流感病毒感染所致的细胞氧化应激损伤、细胞内转录因子(NF-κB和AP-1)转录活性及前炎症细胞因子IL-8释放的影响.方法 甲型流感病毒H3N2作为刺激因素,以DCFH-DA为探针,流式细胞仪检测细胞内活性氧(iROS)产生水平.利用双荧光素酶顺式报告系统,检测人参皂苷Rg1和Rb1对NF-κB-luc及AP-1-luc相对荧光素酶值的影响.RT-PCR法进一步验证人参皂苷Rg1和Rb1对IL-8 mRNA表达水平的影响.结果 病毒感染后细胞中ROS产生增加45%～55%,而给予有效浓度人参皂苷Rg1和Rb1后,荧光强度降低,与正常细胞内自由基含量基本相同.通过NF-κB及AP-1双荧光素酶报告系统检测发现,与正常对照组比较,病毒感染的细胞中NF-κB及AP-1荧光素酶报告活性明显升高;与病毒损伤组比较,人参皂苷Rg1、Rb1治疗组NF-κB及AP-1荧光素酶报告活性明显受到抑制.RT-PCR结果显示人参皂苷Rg1和Rb1能明显抑制病毒诱导的IL-8 mRNA表达水平的变化,使之趋近于正常对照组水平.结论 人参皂苷Rg1和Rb1可拮抗病毒感染细胞中ROS产生水平、降低氧化应激敏感的信号传导通路NF-κB及AP-1的转录活性,并抑制二者下游靶基因IL-8表达.     

Wnt7a/β-连环蛋白/自身免疫调节因子信号通路参与1型糖尿病的发生

目的 探讨NOD/Ltj小鼠自发1型糖尿病（T1D）过程中,胸腺内Wnt信号通路、自身免疫调节因子(AIRE)及T1D组织特异性抗原（TSAs）胰岛素2（Ins2）、谷氨酸脱羧酶67（GAD67）表达与T1D发生的关系。 方法 60只雌性 NOD/Ltj 小鼠分3组：3周组、16周未发病组及16周发病组,每组20只;非空腹血糖值连续2次≥ 11.1 mmol/L 视为发生T1D。胰腺HE染色观察胰岛炎发生情况,抗Ins、CD45免疫组织化学染色显示胰岛β细胞或浸润炎性细胞;Western blotting和Real-time PCR检测胸腺Wnt7a、β-catenin、AIRE、Ins、GAD67蛋白水平和mRNA表达;流式细胞术分析胸腺T细胞比例。 结果 1. 随着T1D发生,胰岛组织结构破坏,大量淋巴细胞浸润,残存胰岛细胞减少;Ins+胰岛β细胞周围见大量CD45+细胞聚集。2. 随年龄的增加,胸腺Wnt7a、β-连环蛋白（catenin)、AIRE、Ins和GAD67蛋白水平和mRNA表达降低;同周龄发病组小鼠与未发病组小鼠相比,胸腺Ins表达下降。3. 与3周组相比,16周未发病组CD4、CD8单阳性T细胞比例降低;16周发病组CD4、CD8单阳性T细胞比例升高,CD4、CD8双阳性T细胞比例降低。 结论 Wnt7a/β-catenin信号通路可能通过调控AIRE表达,下调T1D相关TSAs表达,参与T1D发生发展。     

C1型尼曼-匹克病小鼠肝脏功能及病理变化

目的 探讨晚期（P60）Npc1^-/-小鼠肝脏功能和病理变化,为C1型尼曼-匹克病（NPC1）患者肝脏的病理发生及临床治疗提供实验依据。 方法 小鼠称重后,眼内眦取血检测血清中乳酸脱氢酶（LDH）、丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）的活性变化,评价Npc1^-/-小鼠的肝功能变化;取肝组织进行石蜡和冷冻切片,通过HE染色和油红O染色评估肝脏组织的形态变化和脂肪储存情况,以及Masson染色评估肝脏组织胶原沉积情况;Real-time PCR和Western blotting分别检测肝脏组织促炎症因子,白细胞介素（IL）-1β、IL-6和肿瘤坏死因子（TNF）-α的mRNA和蛋白水平表达情况;TUNEL染色评估肝脏组织凋亡情况。 结果 与Npc1^+/+小鼠相比,Npc1-/-小鼠的体重及肝脏系数显著降低（P<0.001）;LDH、ALT及AST活性显著升高（P<0.001）;HE染色发现,Npc1^-/-小鼠肝脏组织形态改变明显,出现大量泡沫细胞;油红O染色显示,Npc1^-/-小鼠肝脏脂肪含量显著降低;Real-time PCR显示,Npc1^-/-小鼠肝脏组织IL-1β、IL-6和TNF-α表达均显著升高（P<0.01,P<0.05和P<0.001）,同时,Western blotting也显示,3个因子的蛋白表达均显著升高（P<0.05,P<0.05和P<0.01）,证实Npc1-/-小鼠肝脏晚期发生炎症反应;Masson染色未发现Npc1^-/-小鼠肝脏纤维化的发生;TUNEL染色显示,Npc1^-/-小鼠肝脏组织凋亡细胞数量增加。结论 Npc1基因突变导致肝脏组织形态发生改变,大量的巨噬细胞聚集引发炎症反应,而炎症反应的发生可能是引起肝脏细胞凋亡和肝功能受损的重要途径之一。     

木犀草素对重症急性胰腺炎小鼠胰腺的保护作用及可能的分子机制#br#

目的 探讨木犀草素对重症急性胰腺炎（SAP）小鼠胰腺的保护作用及其可能的分子机制。方法 将60只SPF级健康雄性C57BL/6小鼠随机分为3组,对照组、SAP模型组和治疗组,每组各20只。采用雨蛙素法构建模型,成功构建SAP模型后,应用ELASA法检测脂肪酶、淀粉酶、血红素加氧酶（HO)-1、肿瘤坏死因子（TNF）-α、丙二醛（MDA）及超氧化物歧化酶（SOD）水平。使用Western blotting和Real-time PCR测定各组小鼠核因子（NF）-κB、P38及p-P38 蛋白和mRNA水平。结果 与对照组比较,模型组和治疗组小鼠胰腺干湿重比、脂肪酶及淀粉酶、TNF-α水平、氧化应激指标HO-1及MDA水平均明显升高,SOD水平明显降低（P<0.05）;与模型组小鼠比较,治疗组小鼠胰腺干湿重比、脂肪酶及淀粉酶,TNF-α、MDA水平均明显降低,HO-1、SOD水平均明显升高（P<0.05）。与对照组比较,模型组和治疗组小鼠NF-κB、p-P38蛋白和mRNA水平明显升高（P<0.05）,P38蛋白和mRNA表达水平无显著变化（P>0.05）;与模型组小鼠比较,治疗组小鼠NF-κB、p-P38蛋白和mRNA水平均明显降低（P<0.05）。结论 木犀草素对SAP小鼠胰腺具有一定的保护作用,其可能的分子机制为缓解炎症应激和氧化应激,下调NF-κB及p-P38 蛋白的表达。     

人参皂苷Rb1改善自噬流抗离体大鼠心脏心肌缺血再灌注损伤

目的通过Langendorff系统构建离体大鼠心肌缺血/再灌注(I/R)损伤模型,探讨人参皂苷Rb1对心肌I/R损伤的保护作用及机制。方法选取健康成年雄性SD大鼠60只,随机分为假手术组、I/R组和人参皂苷Rb1(1、5、10和20μmol/L)预处理组,每组10只。大鼠开胸、结扎主动脉后,取出心脏置于Langendorff系统进行灌流,按照分组情况构建相应模型。采用Lab Chart电生理系统检测心率(HR)、左心室发展压(LVDP)、左室压上升/下降最大速率(±dp/dtmax)等相关心功能指标;采用TTC染色法检测心肌梗死面积;采用Western blotting检测Beclin 1、LC3、p62和Lamp 2表达情况;采用免疫组织化学法检测Beclin 1表达情况。结果人参皂苷Rb1(1、5、10和20μmol/L)改善由I/R损伤导致的LVDP和±dp/dtmax的下降,减少心肌梗死面积,其中10μmol/L浓度人参皂苷Rb1对心功能保护作用最显著(P<0.05)。Beclin 1在I/R组心肌细胞胞质中阳性表达率显著增高,加入人参皂苷Rb1(10μmol/L)后表达量减少(P<0.05)。与sham组相比,在I/R组发现自噬流受损:自噬相关蛋白Beclin 1、LC3和p62表达水平升高,Lamp 2表达水平下调(P<0.05)。加入人参皂苷Rb1(10μmol/L)后上述蛋白的调控作用被反转,自噬流通畅(P<0.05)。结论人参皂苷Rb1预处理通过改善自噬流受损发挥抗大鼠离体心肌I/R损伤的保护作用,其中以10μmol/L浓度的人参皂苷Rb1保护作用最好。     

Interleukin-1 beta promotes sensory nerve regeneration after sciatic nerve injury

Nerve injury brings about axonal disconnection, and thus axonal extension is one of the important steps for nerve regeneration. Expression of the pro-inflammatory cytokine interleukin-1 beta (IL-1beta) is increased at the early stage of nervous system injury, and previously IL-1beta has been reported to promote neurite outgrowth by inhibiting RhoA activity in vitro. However, the effect of IL-1beta on axonal extension in vivo has not been obvious. Now we examine whether IL-1beta takes advantages on sciatic nerve regeneration. Sciatic nerves of rats are transected and sutured, and IL-1beta or PBS is locally administered for 2 weeks. Although IL-1beta does not influence on motor functional recovery, it promotes sensory functional recovery, estimated by toe pinch test, and increases the number and the area of neurofilament-positive axons at 12 weeks compared with PBS. Moreover IL-1beta, which promotes Schwann cell proliferation and thus may inhibit myelination, does not impair remyelination, estimated by myelin basic protein. These findings suggest that IL-1beta may contribute to sensory nerve regeneration following sciatic nerve injury by promoting axonal extension.     

Altered expression of nectin-like adhesion molecules in the peripheral nerve after sciatic nerve transection

Following axotomy several processes involving cell-cell interaction occur, such as loss of synapses, axon guidance, and remyelination. Two recently discovered families of cell-cell adhesion molecules, nectins and nectin-like molecules (necls) are involved in such processes in vitro and during development, but their roles in nerve injury have been largely unknown until recently. We have previously shown that axotomized motoneurons increase their expression of nectin-1 and nectin-3 and maintain a high expression of necl-1. We here investigate the expression of potential binding partners for motoneuron nectins and necls in the injured peripheral nerve. In situ hybridization (ISH) revealed a decreased signal for necl-1 mRNA in the injured nerve, whereas no signal for necl-2 was detected before or after injury. The signals for necl-4 and necl-5 mRNA both increased in the injured nerve and necl immunoreactivity displayed a close relation to axon and Schwann cell markers. Finally, signal for mRNA encoding necl-5 increased in axotomized spinal motoneurons. We conclude that peripheral axotomy results in altered expression of several necls in motoneurons and Schwann cells, suggesting involvement of the molecules in regeneration.     

芦丁对丙烯酰胺致大鼠坐骨神经髓鞘损伤的保护作用

目的 通过观察芦丁(Rut)对丙烯酰胺(ACR)染毒大鼠坐骨神经髓鞘结构、髓鞘碱性蛋白(MBP)及髓鞘相关糖蛋白(MAG)表达的变化,探讨Rut对ACR致大鼠坐骨神经髓鞘损伤的保护作用.方法 成年SD雄性大鼠36只,随机分为4组:对照组(control,给予ddH2O)、20 mg/kg ACR染毒组(ACR)、100...     

Neuroprotective effect of ginsenoside Rb1 on glutamate-induced neurotoxicity: With emphasis on autophagy

Ginsenoside Rb1 has been demonstrated with neuroprotective effects, but the mechanisms remain unclear. This study aimed to probe the effects and mechanisms of ginsenoside Rb1 on activation of autophagy in glutamate-injured neurons. Ginsenoside Rb1 of exponential concentrations (1.2, 12, 120 μM) or autophagy inhibitor 3-methyladenine (5 mM) was added to culture medium for cortical neurons after being treated with glutamate. Cell viability was measured by MTT assay. Autophagosomes formation was observed with transmission electron microscope. Autophagy marked protein LC3 was detected with immunofluorescence and visualized under laser confocal microscopy. Changes of autophagy related protein Beclin-1 were measured with Western blot. We found that ginsenoside Rb1 protected cortical neurons from glutamate-induced cell injury. Autophagy was activated after glutamate treatment, with both autophagosomes and punctate LC3 increased significantly compared with control. Beclin-1 was elevated in glutamate-treated cells. Formation of autophagosome and punctate LC3 was attenuated by ginsenoside Rb1. The level of Beclin-1 in ginsenoside Rb1 treated cells was simultaneously decreased compared with glutamate-treated cells. These results suggested that inhibition of autophagy could be responsible for neuroprotective effects of ginsenoside Rb1 in glutamate-induced injury. Down-regulation of Beclin-1 may play an important role in this process.     

Regulatory expression of Neurensin-1 in the spinal motor neurons after mouse sciatic nerve injury

Axonal regeneration after crush injury of the sciatic nerve has been intensely studied for the elucidation of molecular and cellular mechanisms. Neurite extension factor1 (Nrsn1) is a unique membranous protein that has a microtubule-binding domain and is specifically expressed in neurons. Our studies have shown that Nrsn1 is localized particularly in actively extending neurites, thus playing a role in membrane transport to the growing distal ends of extending neurites. To elucidate the possible role of Nrsn1 during peripheral axonal regeneration, we examined the expression of Nrsn1 mRNA by in situ hybridization and Nrsn1 localization by immunocytochemistry, using a mouse model. The results revealed that during the early phase of axonal regeneration of motor nerves, Nrsn1 mRNA is upregulated in the injured motor neuron. Nrsn1 is localized in the cell bodies of motor neurons and at the growing distal ends of regenerating axons. These results indicate that Nrsn1 plays an active role in axonal regeneration as well as in embryonic development.     

坐骨神经损伤后长链非编码RNA的聚类分析及长链非编码RNA MX1对大鼠雪旺细胞迁移、增殖能力的影响

目的 探讨坐骨神经损伤后长链非编码RNA（LncRNA）差异表达的基因,以及LncRNA MX1对大鼠雪旺细胞迁移、增殖能力的影响。方法 选取10周龄无特定病原体级雄性SD大鼠24只,随机分为0 d（T0）、3 d（T1）、7 d（T2）和14 d（T3）4组,每组6只,建立坐骨神经损伤动物模型。分别于模型建立后第0、3、7、14天取相应组大鼠坐骨神经损伤处的残端组织提取RNA,制备RNA基因芯片进行Heatmap聚类分析,筛选出各个时间点发生差异表达的基因,并选择其中差异表达显著的基因LncRNA MX1。培养iCell-r030大鼠雪旺细胞,分为对照组、Control siRNA组（siRNA组）和LncRNA MX1 siRNA组（siRNA-MX1组）,使用相应试剂进行转染。转染后采用实时荧光定量聚合酶链反应（qRT-PCR）检测3组雪旺细胞的LncRNA MX1mRNA表达情况,采用Transwell小室检测雪旺细胞的迁移能力,采用5-乙炔基-2'-脱氧尿苷（EDU）实验检测雪旺细胞的增殖能力。结果 各组大鼠均造模成功,实验过程中无大鼠死亡。大鼠损伤坐骨神经组织LncRNA差异基因Heatmap聚类分析的热图显示,与T0组比：T1组共3 066个LncRNA基因发生差异性表达,其中1 634个LncRNA基因表达上调,1 432个LncRNA基因表达下调;T2组共2 498个LncRNA基因发生差异性表达,其中1 634个LncRNA基因表达上调,864个LncRNA基因表达下调;T3组3 567个LncRNA基因发生差异性表达,其中有1 643个LncRNA基因表达上调,1 924个 LncRNA基因表达下调。各组差异表达的LncRNA基因中LncRNA MX1的差异倍数数值较大,差异表达显著。大鼠雪旺细胞qRT-PCR结果显示,转染LncRNA MX1 siRNA后,siRNA-MX1组LncRNA MX1的相对表达量为1.0±0.2,低于对照组的2.3±0.2和siRNA组的2.2±0.2,差异有统计学意义（F=78.47,P<0.001）;而对照组和siRNA组组间差异无统计学意义（P>0.05）。迁移、增殖试验结果显示,siRNA-MX1组细胞迁移数量为（24.1±4.2）个、EDU阳性细胞与DAPI阳性细胞的比率为27.5%±2.8%,低于对照组的（50.3±7.8）个、44.1%±7.2%和siRNA组的（49.2±6.2）个、41.8%±7.0%,差异均有统计学意义（F=93.15、121.26,P值均<0.001）;而对照组和siRNA组间差异均无统计学意义（P值均>0.05）。结论 大鼠坐骨神经损伤后LncRNA MX1差异表达显著,下调LncRNA MX1在大鼠雪旺细胞中的表达可显著降低细胞的迁移、增殖能力。     

Oxidized galectin-1 advances the functional recovery after peripheral nerve injury

Oxidized galectin-1 has been shown to promote axonal regeneration from transected-nerve sites in an in vitro dorsal root ganglion (DRG) explant model as well as in in vivo peripheral nerve axotomy models. The present study provides evidence that oxidized galectin-1 advances the restoration of nerve function after peripheral nerve injury. The sciatic nerve of adult rats was transected and the distal nerve was frozen after being sutured into a proximal site with four epineurial stitches. An osmotic pump delivered oxidized galectin-1 peripherally to the surgical site. Functional recovery was assessed by measurement of the degree of toe spread of the hind paw for 3 months after the sciatic nerve lesion. The recovery curves of toe spread in the test group showed a statistically significant improvement of functional recovery after day 21 by the application of oxidized recombinant human galectin-1 (rhGAL-1/Ox) compared to the control group. This functional recovery was supported by histological analysis performed by light microscopic examination. The regenerating myelinated fibers at the site 21 mm distal to the nerve-transected site were quantitatively examined at 100 days after the operation. The frequency distribution of myelinated fiber diameters showed that exogenous rhGAL-1/Ox increased the number and diameter of regenerating myelinated fibers; the number of medium-sized (6–11 μm in diameter) fibers increased significantly (P < 0.05). These results indicate that oxidized galectin-1 promotes the restoration of nerve function after peripheral nerve injury. Thus, rhGAL-1/Ox may be a factor for functional restoration of injured peripheral nerves.     

睾酮对小鼠坐骨神经损伤后脊髓前角运动神经元的保护作用

目的探讨睾酮对坐骨神经损伤后脊髓运动神经元的保护作用。方法12只性成熟C57雄性小鼠随机分为:芝麻油对照组(n=6)和睾酮实验组(n=6)。采用单侧坐骨神经切断损伤模型,手术后分别隔日皮下注射芝麻油和睾酮。两周后通过尼氏染色统计腰骶髓坐骨神经损伤侧的前角运动神经元数量和截面积。结果睾酮实验组腰骶髓前角运动神经元状态要好于芝麻油对照组,胞体饱满,突起较多。神经元数量和平均截面积明显大于芝麻油对照组(P0.01)。结论坐骨神经损伤后,睾酮对支配该神经的运动神经元具有明显的保护作用,增加存活运动神经元的数量和截面积。