miR-144-3p对前列腺癌PC3细胞增殖和侵袭的影响及可能机制

目的 探讨miR-144-3p对前列腺癌PC3细胞增殖和侵袭的影响及可能机制.方法 利用脂质体介导的方法进行转染,将前列腺癌PC3细胞分为空白组(未进行转染)、miR-144-3p阴性对照组(转染无义序列)和miR-144-3p模拟物组(转染miR-144-3p模拟物),采用实时定量PCR验证转染效率,Western ...     

过表达miR-144-3p减轻AngⅡ诱导的HUVEC损伤

目的 探讨miR-144-3p对AngⅡ诱导的人脐静脉内皮细胞(HUVEC)增殖、侵袭、凋亡和ROS水平的影响。方法 将细胞分为对照组(control)、模型组(AngⅡ)、阴性对照组(AngⅡ+转染miR-144-3p NC)和实验组(AngⅡ+转染miR-144-3p mimic)。PCR验证转染效率;MTT法检测细胞增殖;Transwell小室法检测细胞侵袭;凋亡试剂盒和流式细胞测量术检测细胞凋亡;流式细胞测量术检测细胞内活性氧(ROS)水平。结果 与对照组相比,模型组细胞的增殖和侵袭能力显著下降,而凋亡率和细胞内ROS水平显著上升(P<0.05);而实验组细胞上述指标均可得到一定程度的缓解(P<0.05)。结论 过表达miR-144-3p能够有效减轻由AngⅡ诱导的HUVEC增殖、侵袭能力,以及降低AngⅡ诱导的HUVEC细胞凋亡率和ROS水平。     

人参皂苷Rg1调节miR-144-3p/FPR2/p38信号通路对实验性脑出血大鼠血脑屏障损伤和神经炎症的影响

目的：探讨人参皂苷Rg1调节miR-144-3p对实验性脑出血大鼠神经炎症和血脑屏障损伤的影响,以及对甲酰基肽受体2(FPR2)/p38通路的调控作用。方法：90只SD大鼠随机分为对照组、脑出血组、人参皂苷Rg1低剂量组（10 mg/kg）、人参皂苷Rg1高剂量组（40 mg/kg）、人参皂苷Rg1高剂量+ago-miR-144-3p组（40 mg/kg人参皂苷Rg1+ago-miR-144-3p）,每组18只,除对照组外均通过右侧尾状核注射胶原酶Ⅱ法构建实验性脑出血大鼠模型,按照各组要求腹腔注射给药以及脑内注射给药。对大鼠神经功能损伤进行评分;干湿比重法测定大鼠脑含水量;ELISA检测大鼠脑组织匀浆TNF-α、IL-6、IL-1β水平;电镜观察脑水肿周围超微结构;伊文思蓝（EB）法测定大鼠血脑屏障通透性;qRT-PCR与Western blot测定miR-144-3p/FPR2/p38通路表达。结果：与对照组相比,脑出血组大鼠血脑屏障损伤加重,大鼠神经功能损伤评分、脑含水量、脑组织匀浆miR-144-3p、TNF-α、IL-6、IL-1β、p38 mRNA、p-p38/p38表达增加...     

miR-186-5p修饰骨髓间充质干细胞通过下调FZD3对脊髓损伤大鼠具有神经保护作用

目的 探讨miR-186-5p修饰的骨髓间充质干细胞对脊髓损伤大鼠的神经保护作用及可能机制.方法 40只SD大鼠随机分为假手术组(Sham组)、脊髓损伤模型组(SCI组)、骨髓间充质干细胞移植组(BMSCs组)和miR-186-5p修饰的骨髓间充质干细胞移植组(miR+BMSCs组),每组10只;除了Sham组,其余三组通过Allen's法建立SCI大鼠模型,移植后第1、7、14、21天对各组大鼠进行运动功能(BBB)评分;HE染色观察各组大鼠脊髓损伤病理学变化;IF检测NeuN表达情况;ELISA检测NT-3含量变化;利用qRT-PCR检测各组大鼠miR-186-5p的表达;荧光素酶实验验证miR-186-5p与FZD3的关系;Western blot方法检测损伤脊髓组织中的FZD3、β-catenin、c-Myc、cyclinD1的表达水平变化.结果 与SCI组相比,BMSCs组和miR+BMSCs组的BBB评分、损伤脊髓组织中NeuN的表达、NT-3的表达以及β-catenin、c-Myc、cyclinD1的蛋白表达均明显升高(P＜0.05),FZD3的蛋白表达明显下降(P＜0.05).FZD3被预测并确认为miR-186-5p的靶基因.与BMSCs组相比,miR+BMSCs组的BBB评分、损伤脊髓组织中NeuN的表达、NT-3的表达以及β-catenin、c-Myc、cyclinD1的蛋白表达显著升高(P＜0.05),FZD3的蛋白表达呈下降趋势(P＜0.05).结论 miR-186-5p修饰的骨髓间充质干细胞移植可通过下调FZD3对SCI大鼠的神经提供保护作用.     

miR-27b-3p通过靶向抑制HIF1AN调控颈脊髓损伤后骨质疏松症大鼠的成骨分化

目的 探讨miR-27b-3p在颈脊髓损伤后骨质疏松症(CSCI-OP)发展中的作用与机制。方法 定量PCR检测30例CSCI-OP患者及50例健康体检者外周血中miR-27b-3p的表达。BMP2诱导骨髓间充质干细胞(MSCs)成骨,采用定量PCR检测MSCs中miR-27b-3p和成骨相关基因的mRNA水平。使用miR-27b-3p mimic过表达或使用miR-27b-3p inhibitor下调miR-27b-3p后检测miR-27b-3p的mRNA水平,探讨miR-27b-3p对MSCs成骨相关基因的调控作用。用茜素红染色检测过表达miR-27b-3p后MSCs的成骨能力。双荧光素酶报告基因检测验证miR-27b-3p与HIF1AN的结合情况。通过挽救实验验证miR-27b-3p是否可以通过靶向HIF1AN调控骨质疏松症的发展。建立CSCI-OP大鼠模型验证miR-27b-3p和HIF1AN的表达,micro-CT观察miR-27b-3p mimic对CSCI-OP大鼠股骨组织骨量的影响。结果 CSCI-OP组患者外周血中miR-27b-3p的表达低于对照组(P<0.0...     

miR-28-3p通过调控Notch表达影响子宫内膜癌细胞的增殖和凋亡

目的:探讨微小RNA-128-3p(miR-128-3p)对子宫内膜癌(EC)细胞增殖和凋亡的影响及作用机制.方法:培养人子宫内膜血管内皮细胞hEEC和EC细胞系HEC-1A、Ishikawa和AN3CA,RT-qPCR检测细胞中miR-128-3p和Notch1 mRNA表达水平,Western blot法检测细胞中...     

miR-141-3p、PD-L1及巨噬细胞在子宫内膜异位症中的表达及相关性研究

目的 探讨miR-141-3p、PD-L1及M1、M2型巨噬细胞在子宫内膜异位症 （Endometriosis,EMs） 中的表达及其临床意义。方法 选取2021年10月-2022年7月,因EMs在石河子大学第一附属医院妇科行腹腔镜手术或开腹手术的患者30 例为EMs组,同期选取非EMs患者因子宫肌瘤行诊断性刮宫或子宫全切术的子宫内膜组织30例为对照组,术后病理证实均为增生期子宫内膜。通过qRT-PCR检测子宫内膜组织中miR-141-3p以及PD-L1的表达;通过免疫组化检测子宫内膜组织中 M1型巨噬细胞表面标志物CD86,M2型巨噬细胞表面标志物CD206的表达,并应用Image J软件对免疫组化结果进行平均光密度 （Average Optical Density,AOD） 的检测。通过 Person 或 Spearman 相关检验分析 miR-141-3p、PD-L1、CD86 及 CD206 之间相关性。结果 （1） miR-141-3p 在 EMs 组在位内膜、异位内膜中的表达低于对照组子宫内膜 （P=0.000 5; P＜0.000 1）,且在异位内膜中表达最低。（2）PD-L1在EMs组在位内膜、异位内膜中的表达高于对照组子宫内膜（P=0.013 7; P=0.000 3）,且在异位内膜中表达最高。（3）在EMs异位内膜中miR-141-3p与PD-L1的表达呈负相关（r =-0.648 9,P=0.000 1）。 （4） CD86在EMs组在位内膜、异位内膜中的表达低于对照组子宫内膜 （P=0.047 2;P=0.001 0）。（5） CD206在EMs组在位内膜、异位内膜中的表达高于对照组子宫内膜 （P=0.043 4;P＜0.000 1）,且在异位内膜中表达最高。（6） PD-L1与M1型巨噬细胞标志物 CD86 在 EMs 异位内膜中的表达呈负相关 （r =-0.440 8,P=0.014 8）。（7） PD-L1 与 M2 型巨噬细胞标志物 CD206在EMs异位内膜中的表达呈正相关 （r =0.598 1,P=0.000 5）。结论 EMs患者中miR-141-3p表达降低,PD-L1表达升高,巨噬细胞从M1型向M2型极化,且随病情进展而改变。     

MiRNA-125a-5p对大鼠脊髓损伤后血脊髓屏障及运动功能的影响

目的:通过干预大鼠脊髓中miRNA-125a-5p的表达量,探讨miRNA-125a-5p在脊髓损伤(SCI)后对血脊髓屏障(BSCB)的作用及对大鼠运动功能的影响。方法:SD大鼠随机分为假手术组(Sham组)、脊髓损伤组(SCI组)、miRNA空载组(NC组)和miRNA-125a-5pagomir鞘内注射组(miRNA组)。RT-PCR检测miRNA-125a-5p在各种大鼠脊髓中的表达,免疫印迹和免疫荧光实验检测脊髓微血管内皮细胞间紧密连接蛋白(ZO-1)表达,尼氏染色观察脊髓前角运动神经元的数量以及通过BBB评分评价大鼠运动功能恢复。结果:MiRNA组的miRNA-125a-5p的相对表达量明显高于SCI组,且ZO-1的mRNA的相对表达量和相对蛋白质表达量较SCI组和显著增加。MiRNA组的脊髓前角运动神经元相对数量明显多于SCI组。MiRNA组大鼠脊髓损伤后1 d、3 d、7 d、14 d、21 d和28 d运动功能恢复明显优于SCI组。结论:MiRNA-125a-5p可以有效保护脊髓损伤大鼠的血脊髓屏障功能并促进运动功能恢复。     

仙茅苷调控miR-1247-3p表达对高糖诱导的肾小管上皮细胞炎症反应的影响北大核心CSCD

目的:探讨仙茅苷对高糖诱导的肾小管上皮细胞炎症反应的影响及分子机制。方法:肾小管上皮细胞HK-2随机分为正常对照组(Con)、高糖组(HG)、HG+仙茅苷低、中、高剂量组、HG+miR-NC组、HG+miR-1247-3p组、HG+仙茅苷+antimiR-NC组、HG+仙茅苷+anti-miR-1247-3p组;ELISA检测TNF-α、IL-6水平;流式细胞术检测细胞凋亡;RT-qPCR检测miR-1247-3p水平。结果:仙茅苷低、中、高剂量处理后,高糖诱导的肾小管上皮细胞培养液中IL-6、TNF-α水平随药物浓度的增加逐渐降低,细胞凋亡率逐渐降低,miR-1247-3p表达水平逐渐升高(P<0.05)。与HG+miR-NC组相比,miR-1247-3p过表达肾小管上皮细胞培养液中IL-6、TNF-α水平降低,细胞凋亡率降低(P<0.05)。下调miR-1247-3p表达可逆转仙茅苷对高糖诱导的肾小管上皮细胞炎症反应作用。结论:仙茅苷通过上调miR-1247-3p表达抑制高糖诱导的肾小管上皮细胞炎症损伤。     

LncRNA TUG1靶向miR-141-3p影响甲状腺癌细胞的增殖和侵袭

目的 检测LncRNA TUG1在甲状腺癌细胞中的表达,初步探讨LncRNA TUG1对甲状腺癌细胞增殖和侵袭的影响及机制。方法 采用qRT-PCR法检测甲状腺癌B-CPAP、TPC-1细胞株中LncRNA TUG1和miR-141-3p的表达水平,应用生物信息学预测lncRNA TUG1和miR-141-3p的靶向关系,双荧光素酶报告基因实验进行验证。将lncRNA TUG1干扰序列转染TPC-1细胞,应用qRT-PCR法检测lncRNA TUG1和miR-141-3p的表达,MTT法检测各组TPC-1细胞增殖能力,Transwell实验检测各组TPC-1细胞的侵袭能力。结果 与正常甲状腺上皮细胞相比,BCPAP、TPC-1中LncRNA TUG1表达水平明显升高（P<0.05）,miR-141-3p表达水平明显下降（P<0.05）,生物信息学分析及双荧光素酶实验结果显示,lncRNA TUG1可以靶向调控miR-141-3p。转染TUG1干扰序列能够降低TPC-1细胞lncRNA TUG1的表达,上调miR-141-3p的表达（P<0.05）;沉默lncRNA T...     

Effect of melatonin on the functional recovery from experimental traumatic compression of the spinal cord

Spinal cord injury is an extremely severe condition with no available effectivetherapies. We examined the effect of melatonin on traumatic compression of the spinalcord. Sixty male adult Wistar rats were divided into three groups: sham-operatedanimals and animals with 35 and 50% spinal cord compression with a polycarbonate rodspacer. Each group was divided into two subgroups, each receiving an injection ofvehicle or melatonin (2.5 mg/kg, intraperitoneal) 5 min prior to and 1, 2, 3, and 4 hafter injury. Functional recovery was monitored weekly by the open-field test, theBasso, Beattie and Bresnahan locomotor scale and the inclined plane test.Histological changes of the spinal cord were examined 35 days after injury. Motorscores were progressively lower as spacer size increased according to the motor scaleand inclined plane test evaluation at all times of assessment. The results of the twotests were correlated. The open-field test presented similar results with a lesspronounced difference between the 35 and 50% compression groups. The injured groupspresented functional recovery that was more evident in the first and second weeks.Animals receiving melatonin treatment presented more pronounced functional recoverythan vehicle-treated animals as measured by the motor scale or inclined plane.NADPH-d histochemistry revealed integrity of the spinal cord thoracic segment insham-operated animals and confirmed the severity of the lesion after spinal cordnarrowing. The results obtained after experimental compression of the spinal cordsupport the hypothesis that melatonin may be considered for use in clinical practicebecause of its protective effect on the secondary wave of neuronal death followingthe primary wave after spinal cord injury.     

Transplantation of mononuclear cells from human umbilical cord blood promotes functional recovery after traumatic spinal cord injury in Wistar rats

Cell transplantation is a promising experimental treatment for spinal cord injury. The aim of the present study was to evaluate the efficacy of mononuclear cells from human umbilical cord blood in promoting functional recovery when transplanted after a contusion spinal cord injury. Female Wistar rats (12 weeks old) were submitted to spinal injury with a MASCIS impactor and divided into 4 groups: control, surgical control, spinal cord injury, and one cell-treated lesion group. Mononuclear cells from umbilical cord blood of human male neonates were transplanted in two experiments: a) 1 h after surgery, into the injury site at a concentration of 5 x 10⁶ cells diluted in 10 µL 0.9% NaCl (N = 8-10 per group); b) into the cisterna magna, 9 days after lesion at a concentration of 5 x 10⁶ cells diluted in 150 µL 0.9% NaCl (N = 12-14 per group). The transplanted animals were immunosuppressed with cyclosporin-A (10 mg/kg per day). The BBB scale was used to evaluate motor behavior and the injury site was analyzed with immunofluorescent markers to label human transplanted cells, oligodendrocytes, neurons, and astrocytes. Spinal cord injury rats had 25% loss of cord tissue and cell treatment did not affect lesion extension. Transplanted cells survived in the injured area for 6 weeks after the procedure and both transplanted groups showed better motor recovery than the untreated ones (P < 0.05). The transplantation of mononuclear cells from human umbilical cord blood promoted functional recovery with no evidence of cell differentiation.     

Passive immunization with tenascin-R (TN-R) polyclonal antibody promotes axonal regeneration and functional recovery after spinal cord injury in rats

Tenascin-R (TN-R) is a neural specific protein and an important molecule involved in inhibition of axonal regeneration after spinal cord injury (SCI). Here we report on rabbit-derived TN-R polyclonal antibody, which acts as a TN-R antagonist with high titer and high specificity, promoted neurite outgrowth and sprouting of rat cortical neurons cultured on the inhibitory TN-R substrate in vitro. When locally administered into the lesion sites of rats received spinal cord dorsal hemisection, these TN-R antibodies could significantly decrease RhoA activation and improve functional recovery from corticospinal tract (CST) transection. Thus, passive immunotherapy with specific TN-R antagonist may represent a promising repair strategy following acute SCI.     

miR-144和miR-502—3p在原发性肝细胞癌术后复发患者中的表达及临床意义

目的探讨miR-144和miR-502-3p在原发性肝细胞癌术后复发患者中的表达及临床意义。方法从我院肝癌数据标本库中挑选82例原发性肝癌深低温冻存组织标本。其中50例早期复发组（术后1年内肝内出现复发病灶）;32例非早期复发组（术后超过2年未出现肝内复发病灶）。运用实时荧光定量PCR验证miR-144、miR-502—3p在两组肝癌组织中的表达水平。结果相对于非早期复发组,miR-144在肝癌早期复发组中表达上调[（43．893±107．890）VS（6．321±6．845）,P=0．018];其在肝癌组织中的表达仅与肝癌术后早期复发有关（P〈0．05）。而miR-502—3p在肝癌早期复发组中表达下调[（6．702±9．775）VS（26．467±39．613）,P=0．009];其在肝癌组织中的表达与肿瘤直径、肝癌术后早期复发、脉管癌栓、肝硬化、Edmonson病理分级有关（P〈0．05）。结论miR-144、miR-502-3p与肝癌的早期复发转移密切相关,并且可能是肝癌早期复发的分子标记物以及未来肝癌靶向治疗的有效靶点。     

The effect of systemic PTEN antagonist peptides on axon growth and functional recovery after spinal cord injury

Knockout studies suggest that PTEN limits the regenerative capacities of CNS axons as a dominant antagonist of PI3 kinase, but the transgenic approach is not feasible for treating patients. Although application of bisperoxovanadium may block PTEN function, it is a general inhibitor of phosphotyrosine phosphatases and may target enzymes other than PTEN, causing side effects and preventing firm conclusions about PTEN inhibition on regulating neuronal growth. A pharmacological method to selectively suppress PTEN post-injury could be a valuable strategy for promoting CNS axon regeneration. We identified PTEN antagonist peptides (PAPs) by targeting PTEN critical functional domains and evaluated their efficacy for promoting axon growth. Four PAPs (PAP 1–4) bound to PTEN protein expressed in COS7 cells and blocked PTEN signaling in vivo. Subcutaneous administration of PAPs initiated two days after dorsal over-hemisection injury significantly stimulated growth of descending serotonergic fibers in the caudal spinal cord of adult mice. Systemic PAPs induce significant sprouting of corticospinal fibers in the rostral spinal cord and limited growth of corticospinal axons in the caudal spinal cord. More importantly, PAP treatment enhanced recovery of locomotor function in adult rodents with spinal cord injury. This study may facilitate development of effective therapeutic agents for CNS injuries.     

促红细胞生成素对大鼠脊髓损伤后caspase-3表达及神经细胞凋亡的影响

目的通过观察重组人红细胞生成素（recombinant human erythropoietin，rHu—EPO）对大鼠急性脊髓损伤后Caspase-3表达及凋亡的影响，探讨其脊髓保护的作用机制。方法60只SD大鼠随机分成3组：假手术组，对照组和治疗组，每组20只，采用Allen’s打击法制成急性脊髓损伤模型。观察药物治疗前后大鼠的神经功能行为，用免疫组化染色检测caspase-3表达，原位脱氧糖核苷酸末端转移酶介导的缺口末端标记法（Tunel法）标记凋亡细胞；比较各组间差别。结果HE，免疫组化染色示EPO治疗组脊髓损伤程度小，神经元细胞破坏少；caspase-3在各时相点的表达明显降低，8h和7dTunel标记凋亡阳性细胞显著减少；大鼠神经功能恢复显著优于对照组（P〈0．01）。结论EPO能下调Caspase-3表达，抑制脊髓神经细胞凋亡，对继发性脊髓损伤有保护作用。     

miR-124 regulates neural stem cells in the treatment of spinal cord injury

Several studies demonstrated that the overexpression of miR-124 in neural stem cells (NSCs) could lead the NSCs to differentiate into neurons and astrocytes, which may be important for functional recovery in spinal cord injury. The present study attempted to explore the potential repairing effect of the NSCs transfected with miR-124 for the rats with spinal cord injury (SCI). NSCs transfected with miR-124 were transplanted into rats by intravenous injection after SCI. The effects of miR-124 on the differentiation of NSCs and the treatment for the SCI-model rats were experimentally investigated. The reduction of cavity volume in focal lesions and Basso–Beattie–Bresnahan (BBB) scores were used as the criteria of functional recovery of the SCI-model rats. Up-regulation of miR-124 promoted the differentiation of NSCs. Transfection of miR-124 in NSCs dramatically increased the percentage of NeuN-positive cells, and reduced the percentage of GFAP-positive cells in vitro and in vivo respectively. All of the rats treated with NSCs transfected with miR-124 achieved the better functional recovery than the ones in NSCs and sham control groups. Furthermore, the systemic delivery of the NSCs transfected with miR-124 resulted in a reduction of lesion cavity volume of SCI-model rats. Thus, Overexpression of miR-124 can promote the differentiation of NSCs and play an important role in the repair of SCI. The utility of intravenous delivery of stem cells regulated with miR-124 to target lesion areas as a prospective therapeutic approach in acute spinal cord injury is very promising in the future.     

Metallothionein-II improves motor function recovery and increases spared tissue after spinal cord injury in rats

After spinal cord injury (SCI), a complex cascade of pathophysiological processes rapidly damages the nervous tissue. The initial damage spreads to the surrounding tissue by different mechanisms, including oxidative stress. We have recently reported that the induction of metallothionein (MT) protein is an endogenous rapid-response mechanism after SCI. Since the participation of MT in neuroprotective processes after SCI is still unknown, the aim of the present study was to evaluate the possible neuroprotective effect of exogenously administered MT-II during the acute phase after SCI in rats. Female Wistar rats weighing 200-250g were submitted to spinal cord contusion by means of a computer-controlled device (NYU impactor). Rats received several doses of MT-II (3.2, 10 and 100μg) at 2 and 8h after SCI. Results of the BBB scale were statistically analysed using an ANOVA of repeated-measures, followed by Tukey's test. Among the three doses tested, only 10 and 100μg were able to significantly increase (p<0.05) BBB scale scores eight weeks after SCI from a mean of 7.88 in the control group, to means of 12.63 and 10.88 for the 10 and 100μg doses of MT-II, respectively. The amount of spared tissue was also higher in the groups treated with 10 and 100μg, as compared to the control group values. Results from the present study demonstrate a significant neuroprotective effect of exogenously administered MT-II. Further studies are needed in order to characterize the mechanisms involved in this neuroprotective action.     

振荡电场刺激治疗脊髓损伤的研究进展

脊髓损伤是一种发病率较高的致残病变.振荡电场刺激可以促进损伤的轴突再生.就近年来振荡电场刺激治疗脊髓损伤的进展进行了综述,包括人体临床试验、联合疗法的应用、治疗领域的拓展以及作用机理上的进展,同时指出了目前研究中存在的问题,并对发展趋势进行了展望.     

Simvastatin treatment improves functional recovery after experimental spinal cord injury by upregulating the expression of BDNF and GDNF

The aim of this study was to determine the therapeutic efficacy of simvastatin treatment starting 1 day after spinal cord injury (SCI) in rat and to investigate the underlying mechanism. Spinal cord injury was induced in adult female Sprague–Dawley rats after laminectomy at T9-T10. Then additionally with sham group (laminectomy only) the SCI animals were randomly divided into 3 groups: vehicle-treated group; 5-mg/kg simvastatin-treated group; and 10-mg/kg simvastatin-treated group. Simvastatin or vehicle was administered orally at 1 day after SCI and then daily for 5 weeks. Locomotor functional recovery was assessed during 8 weeks postoperation by performing open-field locomotor test and inclined-plane test. At the end of study, motor evoked potentials (MEPs) and somatosensory evoked potentials (SEPs) were assessed to evaluate the integrity of spinal cord pathways. Then, the animals were killed, and 1-cm segments of spinal cord encompassing the injury site were removed for histopathological analysis. Immunohistochemistry was performed to observe the expression of brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF) in the spinal cord. Results show that the simvastatin-treated animals showed significantly better locomotor function recovery, better electrophysiological outcome, less myelin loss, and higher expression of BDNF and GDNF. These findings suggest that simvastatin treatment starting 1 day after SCI can significantly improve locomotor recovery, and this neuroprotective effect may be related to the upregulation of BDNF and GDNF. Therefore, simvastatin may be useful as a promising therapeutic agent for SCI.