大鼠脊髓损伤后神经细胞凋亡及相关调控蛋白Caspase-3表达的时空分布

目的 观察大鼠脊髓损伤（SCI）后神经元细胞凋亡和相关调控蛋白Caspase-3表达的时间、空间分布规律。方法 SD大鼠50只,分为假手术组和SCI组,钳夹法建立SCI模型,用结晶紫（CV）染色法、TUNEL法和免疫组织化学方法观察SCI后6h、12h、24h、3d和7d损伤中心到头端0～5.00mm空间范围内脊髓神经细胞存活、凋亡以及相关调控蛋白Caspase-3的表达状况。 结果 CV染色发现,SCI后6h～7d在0～0.50mm空间范围内均未发现存活的神经细胞,在1.00～3.50mm距离内,存活的神经细胞数逐渐增加,4.00mm处达峰值;TUNEL结果发现,SCI后6h～7d在1.05～4.55mm范围内,神经细胞出现凋亡,3d时在2.55mm处,细胞凋亡达高峰,7d时显著减少;免疫组织化学结果发现,SCI后6h～7d在1.10～4.60mm范围内,神经元细胞出现Caspase-3阳性表达,3d在3.10mm处Caspase-3表达达到高峰,7d显著减少。 结论 SCI后,凋亡的神经细胞及其相关调控蛋白Caspase-3的表达有一定的时空分布规律。     

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。     

抑制mTOR通路对局灶性脑缺血再灌注损伤大鼠自噬的影响

目的:应用哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,m TOR)抑制剂Cystatin C,探讨其对局灶性脑缺血再灌注大鼠自噬的影响。方法:成年雄性SD大鼠60只(体质量260~280 g),随机分为假手术组(sham)、缺血再灌注组(I/R)、Cystatin C组(根据不同浓度分为低、中、高3个亚组Ⅰ、Ⅱ、Ⅲ),每组12只。I/R组和Cystatin C组采用线栓法制备大鼠右侧脑缺血再灌注损伤模型。缺血2 h再灌注24 h,观察神经功能缺损评分、测定脑梗死体积;应用Western Blot技术检测损伤脑皮质中自噬标志物LC3-Ⅱ、LC3-Ⅰ和Beclin-1的变化。结果:与I/R组相比,Cystatin CⅠ、Ⅱ组大鼠神经功能缺损评分和脑梗死体积减少,而Cystatin CⅢ组大鼠神经功能缺损评分和脑梗死体积增大。I/R组脑皮质中自噬标志物LC3-Ⅱ/LC3-Ⅰ比值和Beclin-1表达明显升高(P0.05);Cystatin C各组脑皮质中LC3-Ⅱ/LC3-Ⅰ和Beclin-1的表达逐步升高,且与浓度呈正相关。结论:m TOR抑制剂Cystatin C干预脑缺血再灌注大鼠可诱导脑皮质组织自噬,Cystatin CⅠ、Ⅱ组可减轻脑组织损伤,而Cystatin CⅢ组则加重脑组织损伤。     

miR-144-3p对大鼠脊髓损伤后巨噬细胞炎症反应和功能恢复的影响

目的 探究miR-144-3p对脊髓损伤大鼠的巨噬细胞炎症反应和运动功能恢复的影响。方法 分析脊髓损伤大鼠miRNA表达数据集GSE19890中miR-144的表达情况;在ENCORI网站中预测miR-144-3p的靶基因,并通过双荧光素酶报告基因实验验证miR-144-3p与靶基因的结合情况;构建脊髓损伤大鼠模型,采用RT-qPCR和Western blot实验验证损伤区域miR-144-3p和Notch1的变化情况;用miR-144-3p mimics或miR-144-3p NC转染LPS诱导的巨噬细胞或经鞘内注射脊髓损伤的大鼠,探究miR-144-3p对体内外巨噬细胞炎症反应和大鼠运动功能恢复的影响。结果 数据集GSE19890中miR-144在大鼠脊髓损伤7 d时明显下调。Notch1作为miR-144-3p的靶基因被其负调控。miR-144-3p在脊髓损伤大鼠模型损伤7 d时明显下调,而Notch1的表达则明显上调。miR-144-3p能够明显抑制LPS体外诱导的M1型巨噬细胞炎症反应和脊髓损伤导致的体内巨噬细胞炎症反应,并且促进脊髓损伤大鼠的运动功能恢复。结论 miR-144-3p靶向调控Notch1的表达,并且通过抑制巨噬细胞炎症反应来促进大鼠脊髓损伤后运动功能的恢复。     

原位胶原凝胶对大鼠脊髓损伤后功能恢复的影响

目的研究脊髓损伤后原位形成胶原凝胶对神经功能恢复的影响。方法15只健康雌性SD大鼠随机分为胶原组、对照组和假手术组．Allen撞击法制作脊髓损伤模型。用微量注射器将胶原溶液注入损伤部位,在体温作用下让其原位形成凝胶,对照组注入PBS溶液,每周进行运动评分,6周后取脊髓组织进行免疫荧光染色,观察损伤部位的胶质瘢痕和轴突生长情况。结果胶原组大鼠第5周起BBB评分显著高于对照组,免疫荧光显示损伤部位胶质瘢痕少于对照组,且长入损伤部位的轴突也多于对照组。结论原位形成的胶原凝胶能抑制损伤部位胶质瘢痕的形成,并能促进轴突再生长入损伤部位。证明胶原是一种较好的能用于修复脊髓损伤的可注射材料。     

被动运动对脊髓损伤大鼠后肢运动功能及骨骼肌的影响

目的　观察被动运动促进脊髓损伤（Spinal cord injury, SCI）大鼠后肢运动功能恢复和改善骨骼肌萎缩的影响;探讨脑源性神经营养因子（BDNF）对被动运动促进功能恢复和延缓肌萎缩的作用。 方法　将36只健康成年雌性SD大鼠随机分假手术组、对照组（未行运动）,被动运动组（损伤1周后开始被动运动,共4 周）。采用改良的Allen’s法制备SCI模型。术后1 d和1、2、3、4 周通过大鼠Basso-Beattie-Bresnahan(BBB)行为学评分检测各组大鼠的运动功能;术后5周,采用HE染色比较各组大鼠脊髓组织病理变化,观察大鼠后肢腓肠肌的横断面积、直径和形态变化。测量腓肠肌湿重、体重和肌湿重/体重,评价肌萎缩情况;采用Western blots检测腓肠肌中BDNF的表达变化。 结果　被动运动组运动功能明显高于对照组（P<0.05）。损伤5周后,对照组和被动运动组的脊髓组织失去正常形态,神经元数量减少,损伤区大量空洞形成,而被动运动组的变化较对照组轻。对照组腓肠肌湿重、肌湿重/体重、横断面积和直径下降,被动运动组改善上述肌萎缩情况（P<0.05）。与假手术组相比,对照组和被动运动组BDNF表达量增加（P<0.05）,其中被动运动组高于对照组（P<0.05）。 结论　被动运动可能是通过增加SCI后BDNF表达促进损伤后运动功能的恢复,并能有效改善失神经性肌萎缩。     

大鼠脊髓损伤后不同时间自噬相关蛋白beclin-1和神经元超微结构的变化

目的:观察大鼠脊髓腰段全横断损伤后beclin-1及脊髓神经元超微结构的变化。方法:雄性Wistar大鼠随机分成损伤后6 h,1、3、7、14 d和21 d及假手术组共7组。脊髓损伤组用手术刀片横切腰段。电镜观察脊髓损伤以下神经元内超微结构形态学变化,免疫印迹检测beclin-1蛋白的表达。结果:脊髓损伤早期出现自噬体和自噬溶酶体,神经元内细胞器以退行性变化为主,随着时间延长,神经元超微结构出现明显改变;脊髓损伤后6 h,1、3、7、14 d和21 d,与假手术组相比,大鼠脊髓组织中beclin-1蛋白明显增加,差异有统计学意义;脊髓损伤后3 d beclin-1蛋白表达最高,7 d开始降低,21 d降到最低。结论:脊髓腰段全横断损伤后神经元自噬活动增强,beclin-1可反映神经元自噬状态的变化。     

重组人促红细胞生成素对SCI大鼠Akt和p-Akt表达的影响

目的探讨重组人促红细胞生成素(recombinant human erythropoietin,rHuEPO)对脊髓损伤(spinal cord injury,SCI)大鼠Akt与p-Akt表达的影响。方法成年健康Wistar大鼠72只,雌雄不限,按随机数字表法分为假手术组、脊髓损伤组和重组人促红细胞生成素治疗组,参照Nystrom's压迫方法制作大鼠脊髓压迫损伤模型,按照存活时间再分为脊髓损伤6h,12h,24h,3d组。免疫组化和Western blot方法检测Akt、p-Akt在各组大鼠脊髓表达的变化。结果免疫组化和Westernblot结果发现,脊髓Akt、p-Akt蛋白阳性表达的平均光密度值SCI组低于假手术组(P<0.05),重组人促红细胞生成素治疗组显著高于SCI组(P<0.05)。结论 rHuEPO可通过上调Akt、p-Akt蛋白的表达参与脊髓损伤修复。     

白藜芦醇对大鼠脊髓损伤后氧化与抗氧化过程的影响

目的探讨白藜芦醇﹙RES﹚对脊髓损伤﹙SCI﹚后髓过氧化物酶﹙MPO﹚和超氧化物歧化酶﹙SOD﹚活性的影响。方法 2008年2月~2010年8月在武汉大学人民医院动物实验中心将96只SD健康成年雄性大鼠随机分成4组,根据Allen’s法制成中度脊髓损伤模型,术后立即管饲白藜芦醇100mg/kg或甲基强的松龙﹙MPSS﹚100mg/kg;通过比色法观察脊髓损伤8小时、1天、3天及7天后白藜芦醇组脊髓MPO及SOD活性的变化,并与MPSS﹙甲基强的松龙﹚组进行疗效对比。结果在脊髓损伤后8小时、1天、3天及7天白藜芦醇组MPO及SOD活性与损伤组差异均有统计学意义,显示白藜芦醇对脊髓损伤具有明显神经细胞保护作用,而且白藜芦醇组与MPSS组间损伤后1天差异具有统计学意义﹙<0.05﹚。结论白藜芦醇在脊髓损伤后能够有效抑制MPO活性的升高幅度,并提高SOD活性,对损伤后脊髓起保护作用。     

脊髓挫伤速度对颈脊髓原发性损伤影响的实验研究

目的　确定脊髓挫伤速度是脊髓损伤的因素,探讨不同速度的脊髓挫伤对大鼠颈脊髓原发性损伤的影响。  方法    20只成年雄性Sprague-Dawley大鼠随机分为快速组（500 mm/s,n=8）、慢速组（5 mm/s,n=8）和对照组（n=4）。用直径为4 mm的平头圆锥打击头在C5水平产生1.5 mm的挫伤位移。损伤后即行心脏固定,切取以挫伤部位为中心长约1.5 cm的脊髓组织。行连续矢状位冰冻切片。HE染色观察脊髓大体形态,计算出血量。β-APP免疫组化后观察轴索损伤程度。  结果　挫伤后观察到脊髓表面有一带状出血,且快速组出血带颜色更深。快速组挫伤位移为(1.50±0.05) mm,最大力为(5.3±1.2) N;慢速组挫伤位移为(1.51±0.04) mm,最大力为(2.8±0.6) N,两组间最大力的差异有显著性（P=0.001）。HE染色显示脊髓出血大部分都集中在灰质,白质相对较少。快速组脊髓总出血量、灰质出血量和白质出血量分别为0.94、0.71和0.23 mm3,慢速组分别为0.55、0.43和0.12 mm3,其中两组间总出血量和灰质出血量的差异有显著性（P＜0.05）。β-APP免疫组化观察到快速组轴索断裂比慢速组更为严重。  结论　脊髓挫伤速度是影响脊髓原发性损伤的因素,快速的脊髓挫伤导致的原发性脊髓损伤更为严重,导致更多的脊髓出血和轴索断裂。     

表没食子儿茶素没食子酸酯对大鼠脊髓损伤后神经细胞凋亡及Caspase-3表达的影响

目的观察表没食子儿茶素没食子酸酯(EGCG)对脊髓损伤(SCI)大鼠神经元凋亡和凋亡调控蛋白Caspase-3时间、空间表达的影响,探讨其脊髓损伤保护机制。方法 SD大鼠75只,分为假手术组、SCI组、EGCG组(n=25只);钳夹法制作脊髓损伤模型,EGCG组和SCI组损伤后即刻和1h后腹腔注射EGCG(50 mg/kg)和等量生理盐水;用结晶紫(CV)染色法、TUNEL和免疫组织化学方法,观察SCI后6h、12h、24h、3d和7d时间范围内,从损伤中心到头端0~5.00mm空间范围内,EGCG对脊髓神经元存活、凋亡以及相关调控蛋白Caspase-3表达的影响。结果 CV染色发现,SCI后6h~7d,在0~0.50mm空间范围内均未发现存活的神经元,在1.00~4.60mm范围内,EGCG和SCI组相比存活的神经元数明显增加(P0.01);TUNEL结果发现,SCI后6h~7d,在1.05~3.05mm范围内,EGCG与SCI组相比凋亡神经元数明显减少(P0.01);免疫组织化学发现,SCI后6h~7d,在1.10~3.10mm范围内,EGCG与SCI组相比Caspase-3阳性表达的神经元数明显减少(P0.01)。结论 EGCG在一定时间、空间范围内能下调Caspase-3表达,减少神经元凋亡,对继发性SCI有拮抗作用。     

Effects of C3 deficiency on inflammation and regeneration following spinal cord injury in mice

Inflammation can activate the complement system, which in turn enhances inflammation and aggravates secondary injury after spinal cord injury (SCI). As the three complement activation pathways converge at the cleavage of C3, we investigated whether inhibiting complement activation in C3-deficient mice would reduce secondary injury after SCI and improve axon regeneration. Weight-drop contusion injury (5 g, 6 cm) was created in wild-type or C3-deficient mice. Astrocytes (ASTs) activation, TNF-α expression, and axon regeneration were investigated in vivo. In other studies, dorsal root ganglia (DRGs) were co-cultured with mechanically injured ASTs in vitro to evaluate effects on neurite outgrowth. Our results show that, after injury, C3-deficient mice exhibit higher BBB scores than wild-type mice. In addition, ASTs activation was inhibited, TNF-α expression process was delayed in vivo and inhibited in vitro, and nerve fiber regeneration was improved in C3-deficient mice. DRGs co-cultured with mechanically injured ASTs from C3-deficient mice also showed improved neurite outgrowth. We conclude that C3 deficiency can inhibit inflammation through suppressing ASTs activation and TNF-α expression, thereby reducing secondary injury and improving neural regeneration and functional recovery after SCI. The above results suggest that complement inhibition may be a potential therapy to promote central nervous system regeneration by targeting C3.     

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.     

粒细胞集落刺激因子对小鼠急性脊髓损伤的神经保护作用及其机制

目的 探讨粒细胞集落刺激因子（G-CSF）对急性脊髓损伤条件下神经保护作用的具体机制。方法 建立小鼠半切脊髓损伤模型。体内实验于造模成功术后第1天开始,给予G-CSF,连续3天,进行Basso-Beattie-Bresnahan (BBB)评分后处死,取脊髓组织进行免疫荧光及免疫印迹（Western blotting）检测。体外培养神经元,建立机械损伤细胞模型,进行形态学观察及缺口末端标记（TUNEL）染色。结果 G-CSF能够促进急性脊髓损伤后运动功能的修复,粒细胞集落刺激因子受体与核磷蛋白（NPM1     

Olfactory bulb implantation and methylprednisolone administration in the treatment of spinal cord injury in rats

Estimate the effects of methylprednisolone (MP) administration and olfactory bulb (OB) implantation independently and in combination after a spinal trauma model in Wistar rats, evaluated with BBB scale and CBS with remark of inclined plane test and Tarlov scale. Thirty adult rats were divided into six different groups, evaluated before trauma, one day post-surgery and weekly up to six weeks post-lesion. Group A (control); group B (sham) laminectomy without lesion; group C (SCI) lesion only; group D (MP) SCI and MP; group E (OB) SCI and OB implantation; group F (MP/OB) SCI and both therapeutics. Intragroup data at three weeks showed evident significance in groups D, E and F for Tarlov (p = 0.001) and BBB (p < 0.01); groups C, D, E and F for CBS (p < 0.05); and only group D with inclined plane (p < 0.05). On the sixth week differences were present in groups C, D, E, and F for Tarlov, BBB and CBS (p < 0.001); and C and F for inclined plane (p < 0.05). For intergroup analysis any treatment showed differences with Tarlov scale; for BBB and inclined plane, statistical differences were evident in groups E and F; and for CBS only in group F (p < 0.05). Real effects of MP are obtained at immediate follow-up, without notorious augmentation after time. OB improvement is achieved only after weeks. None of these therapies used independently achieve a constant and sustained improvement. Combined treatments were more effective and reached higher functional levels for longer periods of time.     

A型肉毒杆菌神经毒素重链干预大鼠脊髓损伤后蛋白表达的初步研究

目的:初步观察大鼠脊髓损伤模型基础上局部注射小剂量A型肉毒杆菌神经毒素重链(BoNT/A HC)后对局部蛋白表达谱的影响,为探讨BoNT/A HC干预在体神经损伤后相关蛋白表达及其干预神经再生机制提供实验基础。方法:复制大鼠单侧腰段脊髓损伤模型;采用SDS-PAGE及双向电泳观察不同剂量BoNT/A HC(2μg、4μg、6μg和8μg)对脊髓损伤后局部(包括损伤部位及其近头端部分脊髓组织)蛋白表达谱的干预作用。结果:大鼠单侧腰段脊髓损伤2 d时局部脊髓组织结构明显破坏崩解,损伤波及左侧脊髓灰质及白质;脊髓损伤局部SDS-PAGE及考马斯亮蓝染色显示,于损伤同时局部一次性注射不同剂量BoNT/A HC后,某些蛋白表达与单纯损伤组相比明显不同,而与正常组基本一致;双向电泳结果进一步显示,损伤局部注射6μg BoNT/A HC后2 d和20 d时,在不同等电点及不同蛋白分子量水平上,有10余种蛋白表达与单纯损伤组明显不同,呈向正常转化的趋势。结论:大鼠脊髓损伤局部注射BoNT/A HC一定时间可影响损伤局部蛋白表达谱的变化,这种变化呈现由损伤造成的蛋白表达变化被转向正常的趋势。     

Curcumin improves the recovery of motor function and reduces spinal cord edema in a rat acute spinal cord injury model by inhibiting the JAK/STAT signaling pathway

Curcumin, a yellow pigment extracted from Carcuma longa, has been demonstrated to have extensive pharmacological activity in various studies, and it exhibits protective effects on injuries involving a number of human organs. The present study was designed to evaluate the potential effect and underlying mechanism of curcumin on the motor function and spinal cord edema in a rat acute spinal cord injury (SCI) model. The SCI model was induced by a heavy object falling. At 30 min after the SCI was successfully induced, the animals were intraperitoneally given 40 mg/kg curcumin. The Basso, Beattie and Bresnahan scores showed that curcumin moderately improved the recovery of the motor function in the injured rats, and hematoxylin–eosin staining demonstrated the role of this compound in reducing the hemorrhage, edema and neutrophil infiltration of the traumatic spinal cord. Furthermore, curcumin also inhibited the SCI-associated aquaporin – 4 (AQP4) overexpression and glial fibrillary acidic protein (GFAP) and repressed the unusual activation of the JAK/STAT signaling pathway. In conclusion, our data demonstrate that curcumin exhibits a moderately protective effect on spinal cord injury, and this effect might be related to the inhibition of overexpressed AQP4 and GFAP and the activated JAK/STAT signaling pathway. Curcumin may have potential for use as a therapeutic option for spinal cord injuries.     

雷公藤甲素干预脊髓损伤模型Thy-YFP转基因小鼠调节自噬及抑制细胞凋亡

文题释义：细胞自噬：自噬是一种细胞的自我保护机制,通过自噬体-溶酶体途径降解和再循环受损细胞器、有毒物质、错误折叠蛋白质等,在维持细胞稳态方面具有重要作用 转基因小鼠：1974年,Rudolf Jaenisch通过将SV40 病毒的DNA注射到小鼠的囊胚中,创造了第一只携带外源基因的小鼠。后来又有研究人员把Murine leukemia病毒注射到小鼠胚胎得到了能通过生殖系统稳定遗传的小鼠,并且外源基因能在后代中稳定表达。这些能稳定遗传且表达外源基因的小鼠即现在一般意义上所说的转基因小鼠。背景：研究表明,在脑卒中大鼠模型中,雷公藤甲素治疗减少了缺血性病变区域面积、水含量和神经细胞死亡。此外,雷公藤甲素能通过抑制星形胶质细胞增生、小胶质细胞活化和抑制炎症反应促进脊髓损伤修复。 目的：研究雷公藤甲素对Thy-YFP转基因小鼠脊髓损伤后细胞自噬和细胞凋亡的影响,探讨雷公藤甲素对脊髓损伤的保护作用及机制。方法：将60只Thy-YFP转基因小鼠随机分为4组,分别是假手术组、二甲基亚砜组、甲基强的松龙组和雷公藤甲素组。假手术组只进行椎板切除术,不损伤脊髓;其他3组建立脊髓损伤模型。雷公藤甲素组、二甲基亚砜及假手术组小鼠术后立即分别腹腔注射雷公藤甲素[0.2 mg/(kg·d)]或等量5%二甲基亚砜-生理盐水溶液,连续给药7 d;甲基强的松龙组小鼠于术后30 min、6 h、24 h腹腔注射甲基强的松龙溶液(30 mg/kg)。BMS评分检测小鼠运动功能恢复情况,苏木精-染色及Nissl染色法检测各组脊髓组织恢复情况,免疫印迹及免疫荧光染色检测各脊髓组织中自噬相关蛋白Beclin-1、LC3B、p62及凋亡相关蛋白Bcl-2、Bax、caspase-3的蛋白水平。动物伦理获得河北北方学院批准(W20200002)。 结果与结论：①雷公藤甲素及甲基强的松龙组脊髓损伤后运动功能改善,神经细胞死亡减少;②雷公藤甲素处理后自噬相关蛋白LC3B上调,p62降低,细胞凋亡相关蛋白caspase-3和Bax降低,抗凋亡蛋白Bcl-2升高;③结果表明,雷公藤甲素能促进脊髓损伤后运动功能恢复,其机制与促进自噬和抑制凋亡有关。结果提示雷公藤甲素可能对脊髓损伤具有潜在的神经保护作用。 ORCID: 0000-0002-8986-6091(朱宁) 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