甲基强的松龙对大鼠脊髓损伤后神经细胞凋亡的影响及其机理

目的研究甲基强的松龙(MP)对大鼠横断性脊髓损伤(SCI)后神经细胞凋亡的影响及其作用机理.方法60只成年Wistar大鼠随机分成正常对照组、脊髓损伤组和MP治疗组,每组20只,MP治疗组在横断T10脊髓组织后30min经尾静脉给予MP治疗,损伤组和对照组未予任何治疗.MP治疗组和脊髓损伤组大鼠于脊髓损伤后8h、24h、3d和1周取材,采用透射电镜、TUNEL染色观察细胞凋亡情况,采用免疫组织化学染色观察Fas、半胱氨酸蛋白酶(caspase)-8和caspase-3在SCI前后的变化情况,采用改良Tarlov评分方法观察大鼠后肢运动功能.结果SCI后24h大鼠后肢运动功能逐渐恢复,MP治疗组大鼠的后肢运动功能恢复优于损伤组,7d后尤其明显.TUNEL染色和电镜检查证实SCI后8h即有凋亡细胞出现,其中既有神经元也有胶质细胞3d凋亡细胞数达到高峰;7d仍有凋亡细胞存在,但已明显减少;各时间点治疗组凋亡细胞数量明显少于损伤组(P＜0.05).治疗组和损伤组在SCI后8h可以检测到少量的Fas和caspase-8阳性神经元及胶质细胞,Fas和caspase-8的表达在SCI后3d达到高峰,7d表达下降,各时间点治疗组的Fas和caspase-8灰度值明显大于损伤组,二者有显著性差异(P＜0.05).治疗组和损伤组caspase-3的表达在SCI后8h均逐渐增加(与对照组相比),7d达到高峰,治疗组灰度值大于损伤组,但二者无显著性差异.结论MP能抑制大鼠脊髓横断性脊髓损伤后的神经细胞凋亡,但不能推迟细胞凋亡出现的高峰时间;MP抑制细胞凋亡的途径可能通过非特异性抑制Fas和caspase-8的表达来实现.     

大鼠脊髓三种不同损伤后神经细胞凋亡的实验比较

目的了解三种不同脊髓机械性损伤对继发性神经细胞凋亡的影响。方法采用脊髓挫伤、持续性占位、脊髓横断三种大鼠损伤模型,在伤后1、4、7d观察损伤断面神经细胞凋亡现象。结果脊髓挫伤组:灰质三个时间组的凋亡指数波动明显,灰质中凋亡指数4d时最高;白质中凋亡细胞除背侧束外腹侧束也存在;另外细胞凋亡以少突胶质细胞凋亡为主。脊髓持续性占位损伤组:灰质、白质细胞凋亡指数在4d和7d组中差异无显著性意义(P>0.05),白质凋亡细胞在受压的背侧束、外侧束为主。脊髓横断损伤组:灰质、白质在三个时间组中均有大量凋亡细胞。结论大鼠脊髓损伤后神经细胞虽然存在主动死亡(细胞凋亡)方式,但凋亡在时间和部位上与损伤类型、损伤部位、损伤程度有关。     

白细胞介素-10对大鼠脊髓损伤后神经细胞凋亡的影响

目的 观察白细胞介素-10(IL-10)对大鼠脊髓损伤(SCI)后脊髓细胞凋亡的影响,探讨IL-10对脊髓损伤的保护作用。方法 将SD大鼠随机分为3组:单纯SCI组(A组)、IL-10治疗组(B组)及假损伤组(Sham组)。除Sham组不致伤脊髓外,A、B两组应用改良的Allen打击法制作大鼠急性 SCI模型,B组大鼠于 SCI后 30 min腹腔注射 10 μg IL-10,再分别于伤后 12、24、48 h、4、8、16和 24 d应用苏木素-伊红(HE)染色、原位末端脱氧核糖核苷酸转移酶介导的脱氧尿苷三磷酸生物素缺口末端标记技术(TUNEL检测法)及开放野行为评分(BBB评分)观察IL-10治疗后脊髓细胞凋亡的变化及神经功能的恢复情况。结果 假损伤组未见凋亡细胞。A组大鼠伤后 12 h即可见零星的凋亡细胞,至 24 h渐增多,伤后 48 h脊髓组织凋亡细胞率达峰值。B组伤后 24、48 h及4d细胞凋亡率比单纯SCI组明显减少,差异具有显著性(P<0.01或P<0.05)。B组脊髓功能恢复亦比A组有明显提高(P<0.05)。结论 SCI后早期应用IL-10可抑制大鼠脊髓细胞凋亡,从而对脊髓损伤起到保护作用。     

脊髓损伤后急性期甲基强的松龙干预对脊髓神经细胞凋亡的影响

目的:观察脊髓损伤后即刻甲基强的松龙干预治疗对脊髓神经细胞凋亡的影响,探讨该药物促进脊髓神经功能修复的机制。方法:采用改良Allen′s法建立脊髓损伤(SCI)兔动物模型,实验动物随机分为假手术组(S组)36只,单纯损伤组(C组)与MP治疗组(T组)各36只,分别于损伤后8h、24h、72h、7d、14d和28d时随机取6只动物灌注固定取材,HE染色观察损伤区脊髓组织的病理改变,TUNEL法检测各组脊髓标本细胞凋亡情况;分别于损伤后1d、3d、7d、14d及28d观察各组动物运动神经功能情况,包括Rivlin斜板试验和BBB评分。结果:术后C组和T组斜板试验临界角度值和BBB评分值随时间点延长均逐渐升高,损伤7d及之后各时间点,T组均高于C组,但小于S组(P<0.05)。HE染色S组脊髓组织在各时间点未见明显异常;T组及C组损伤后8h、24h及72h时脊髓组织结构紊乱,可见不同程度出血、神经细胞水肿、坏死,灰质中空泡形成,炎症细胞浸润,两组无明显区别;损伤后7d、14d及28d,T组脊髓组织较C组恢复较好,整体损伤程度轻,血肿逐渐吸收,空泡减少,灰质和白质坏死吸收并胶原纤维组织增生,胶质细胞减少,可见较多神经细胞。TUNEL法检测凋亡细胞,S组未发现阳性细胞,C组及T组在损伤后8h可见阳性细胞,24h达到高峰,3d时仍较多,术后7d渐渐减少,14d及28d时阳性细胞数明显降低。两组对比,在损伤后8h、24h、3d及7d四个时间点,T组阳性细胞明显少于C组(P<0.05),14d及28d时两组比较无统计学意义(P>0.05)。结论:MP在脊髓损伤急性期干预治疗,有利于损伤的脊髓神经功能恢复,可能通过抗细胞凋亡机制产生作用。     

褪黑素对大鼠脊髓损伤后神经细胞凋亡的影响

目的 观察褪黑素(melatonin,MT)对大鼠脊髓损伤(spinal cord injury,SCI)后脊髓组织细胞凋亡的影响,探讨其对脊髓损伤的保护作用.方法 成年Wister大鼠66只,随机分为三组Sham组(假手术组)、A组(单纯SCI组)及B组(MT治疗组).Sham组仅切除椎板未损伤脊髓;A、B两组采用改良Allen法制成大鼠SCI模型,术后立即分别腹腔注射等体积无水乙醇、褪黑素(100 mg/kg);Sham组于术后48 h、A和B组于术后8、24、48、72 h和7 d分别进行神经功能评分和测定伤段脊髓组织凋亡细胞数.结果 A组凋亡细胞百分率伤后24 h开始升高,48 h达到高峰,72 h开始下降;B组凋亡细胞百分率伤后24 h、48 h及72 h与A组相比明显减少,差异具有显著性(P＜0.05或P＜0.01);B组神经功能比A组有明显提高(P＜0.05).结论 SCI后应用MT可以抑制脊髓组织神经细胞凋亡,从而对脊髓损伤起保护作用.     

大鼠脊髓急性损伤后神经细胞凋亡及相关基因表达△

目的研究脊髓急性损伤后神经细胞的凋亡及相关基因的表达.方法大鼠脊髓(T8、T9)经中度压迫损伤后,分别在30min、2h、4h、8h、24h、48h、72h、7d、14d和21d处死取材(各时间组n=4).应用HE染色、免疫组化及凋亡细胞原位末端标记法对脊髓组织进行标记.结果损伤4h后,在损伤段及邻近段可见末端标记阳性神经元,损伤段灰质中阳性细胞数8h达高峰,24h白质中阳性胶质细胞数量达高峰.相邻节段阳性细胞数72h达高峰.损伤后P53及Bax大量表达,而Bcl-2仅少量表达.结论脊髓损伤后神经细胞的凋亡是继发损伤期的重要病理变化.     

脊髓急性损伤后神经细胞凋亡的时相和空间分布特点

目的 研究脊髓急性损伤后神经细胞的凋亡及其时相和空间特点。方法 大鼠脊髓（T8,9）经中度压迫损伤后,分别在30min、2h、4h、8h、24h、48h、72h、7d、14d、和21d处死取材（n=4)。应用HE、Nissl染色及凋亡细胞原位末端标记法对脊髓组织进行标记。结果 损伤4h后,在损伤段及邻近段可见末端标记阳性神经细胞,损伤段灰质中阳性细胞数8h达高峰,24h白质中阳性胶质细胞数量达高峰。相邻节段阳性细胞数量在72h达高峰。阳性细胞以白质中胶质细胞为主,主要分布于相邻节段。结论 脊髓损伤后神经细胞凋亡是继发损伤期的重要病理变化,并有其时相和空间分布特点。     

大鼠脊髓损伤中的细胞凋亡及甲基强的松龙的干预作用

目的：探讨脊髓损伤（SCI）继发损伤机制,研究损伤脊髓细胞的凋亡及其意义,观察甲基强的松龙（MP）对细胞凋亡的影响。方法：使用改良Allen法制作大鼠急性SCI模型,实验分3组,假损伤（脊髓未受打击）,损伤组及MP治疗组,采用HE,荧光Hoechst 33342,TUNEL(末端脱氧核苷转移酶介导的脱氧尿苷三磷酸生物素缺口末端标记技术）等技术观察SCI后4h,8h,3d,7d,14d,21d及28d时损伤中心及邻近节段脊髓细胞的凋亡,治疗组损伤后30min给予大剂量MP,比较MP治疗组与损伤组脊髓细胞凋亡的变化,同时平行观察大鼠神经学和组织学恢复情况及两组神经丝蛋白（NF）含量的变化。结果：假损伤组各检测方法未见脊髓细胞凋亡,损伤组大鼠急性SCI后1d开始出现脊髓细胞凋亡,3d达高峰,自损伤中心向头尾端递减分布,持续21d,MP治疗组在伤后3d及7d凋亡脊髓细胞较损伤组显著减少,神经学恢复及组织学评分较损伤组有显著性提高,结论：凋亡是SCI后脊髓神经元死亡的一种重要方式,在继发性损伤中起极为重要的作用。MP的治疗作用可能与其干预SCI后细胞凋亡有关。     

大鼠脊髓急性损务后神经细胞凋亡及相关基因表达

目的：研究脊髓急性损伤后神经细胞的凋亡及相关基因的表达,方法：大鼠脊髓（T8、T9）经中度压迫损伤后,分别在30min,2h,4h,8h,24h,48h,72h,7d,14d和21d处死取材（各间组n=4)。应用HE染色、免疫组化及凋亡细胞原位未端标记法对脊髓组织进行标记。结果：损伤4h后,在损伤段及邻近段可见末端标记阳性神经元,损伤段灰质中阳性细菌数8h达高峰,24h白质中阳性胶质细胞数量达高峰。相邻节段阳性细胞数72h达高峰。损伤后P53及Bax大量表达,而Bcl-2仅少量表达。结论：脊髓损伤后神经细胞的凋亡发损伤期的重要病理变化。     

醛糖还原酶在急性脊髓损伤中的表达及其抑制剂对脊髓细胞凋亡的影响

目的 观察醛糖还原酶(AR)在急性脊髓损伤中的表达和醛糖还原酶抑制剂( ARI)对脊髓细胞凋亡的影响.方法 成年SD大鼠150只,随机分为3组:假手术对照组(Sham组,n=50只),脊髓损伤组(SCI组,n=50只),醛糖还原酶酶抑制剂(依帕司他片,唐林)组(ARI组,n=50只),每组大鼠分别分为3、12、24、48、72h5个时间点.假手术组只做椎板切除术,SCI组和ARI组采用Allen's法制备大鼠脊髓冲击伤模型.苏木素-伊红(HE)染色观察脊髓组织病理变化,双抗体夹心法检测AR含量,原位末端转移酶标记(TUNEL)法检测脊髓组织凋亡.结果 ARI组伤后3、12、24、48、72h损伤l内灰、白质结构破坏程度,空腔形成程度和炎性细胞浸润轻于同时间点的SCI组,假手术组未见到灰质和白质的破坏.Sham组3、12、24、48、72 h脊髓组织中AR含量分别为(10.75±0.47)、(10.61±0.44)、(10.62±0.55)、(10.92±0.49)、(10.57±0.52) U/L,SCI组对应时间点AR含量分别为(12.17±0.65、(14.09±0.61)、(14.58±0.72)、(15.45±0.47)、(15.33±0.29) U/L,ARI组对应时间点AR含量分别为(l0.84±0.21)、(12.70±0.47)、(12.84±0.55)、(12.28±0.54)、(11.95±0.90) U/L,SCI组AR含量在各个时间点均明显高于Sham组和ARI组(P＜0.05),Sham组各时间点很少见到脊髓凋亡细胞,SCI组3、12、24、48、72 h脊髓细胞凋亡率(％)分别为8.45±0.51、27.38±3.19、32.59±3.36、39.04±4.51、23.48±2.40,ARI组对应时间点脊髓细胞凋亡率(％)分别为8.21±0.52、18.69±1.63、22.64±2.18、25.61±3.53、16.48±2.23,SCI组脊髓神经元凋亡率在12、24、48、72 h高于ARI组(P＜0.05).结论 脊髓损伤后AR的表达增高,ARI能降低脊髓神经元细胞的凋亡率.     

Post-traumatic moderate systemic hypothermia reduces TUNEL positive cells following spinal cord injury in rat

STUDY DESIGN: A standardized animal model of contusive spinal cord injury (SCI) with incomplete paraplegia was used to test the hypothesis that moderate systemic hypothermia reduces neural cell death. Terminal deoxynucleotidyl transferase [TdT]-mediated deoxyuridine triphosphate [dUTP] nick-end labeling (TUNEL) staining was used as a marker of apoptosis or cell damage. OBJECTIVE: To determine whether or not moderate hypothermia could have a neuroprotective effect in neural cell death following spinal cord injury in rats. SETTING: Kagawa Medical University, Japan. METHODS: Male Sprague-Dawley (SD) rats (n=39) weighing on average 300 g (280-320 g) were used to prepare SCI models. After receiving contusive injury at T11/12, rats were killed at 24 h, 72 h, or 7 days after injury. The spinal cord was removed en bloc and of examined at five segments: 5 and 10 mm rostral to the center of injury, center of injury, and 5 and 10 mm caudal to the center of injury. Rats that received hypothermia (32 degrees C/4 h) were killed at the same time points as those that received normothermia (37 degrees C/3 h). The specimens were stained with hematoxylin and eosin, and subjected to in situ nick-end labeling (TUNEL), a specific method for visualizing cell death in the spinal cord. RESULTS: At 24 h postinjury, TUNEL positive cells (TPC) decreased significantly 10 mm rostral to center of injury in hypothermic animals compared to the normothermia group. At 72 h post-SCI, TPC also decreased significantly at 5 mm rostral, and 5 and 10 mm caudal to the lesion center compared to normothermic animals. At 7 days postinjury, a significant decrease of TPC was observed at the 5 mm rostral and 5 mm caudal sites compared to normothermic animals. CONCLUSION: These results indicate that systemic hypothermia has a neuroprotective effect following SCI by attenuating post-traumatic TPC.     

黄连素在脊髓损伤中对线粒体的保护作用及机制

目的探讨黄连素对脊髓损伤(SCI)后线粒体氧化损伤的作用和可能机制。方法将36只C57小鼠随机分为假手术组、SCI组(伤后立即腹腔注射10 mg/kg生理盐水)和黄连素组(SCI后立即腹腔注射10 mg/kg黄连素),每组12只。使用PSI-IH脊髓打击器建立小鼠SCI模型,于损伤后24 h处死小鼠,取脊髓组织。使用全自动酶标仪检测各组小鼠脊髓组织线粒体内丙二醛(MDA)、还原型谷胱甘肽(GSH)和超氧化物歧化酶(SOD)的变化;用蛋白质印迹法检测脊髓组织caspase-3、cleaved caspase-3的表达及细胞质内和线粒体内细胞色素C(Cyt C)的表达;用免疫荧光双标染色法检测脊髓组织中神经细胞凋亡情况。结果与假手术组相比,SCI组小鼠脊髓组织线粒体内MDA水平升高,GSH、SOD水平降低;细胞质内Cyt C和脊髓组织中caspase-3、cleaved caspase-3表达水平增高,线粒体内Cyt C表达水平降低;脊髓组织中神经元凋亡比例增高;差异均有统计学意义(P 0.05)。与SCI组相比,黄连素组小鼠脊髓组织线粒体内MDA水平降低,SOD和GSH水平增高;细胞质内Cyt C和脊髓组织中caspase-3、cleaved caspase-3表达水平降低,线粒体内Cyt C表达水平增高;脊髓组织中神经细胞凋亡比例减少;差异均有统计学意义(P 0.05)。结论黄连素可减轻SCI小鼠脊髓组织中神经细胞凋亡,这可能与其抑制线粒体氧化损伤、减少Cyt C释放、降低凋亡蛋白表达有关。     

基于TNFR/RIPK1通路探索紫草素对大鼠脊髓损伤的作用及机制

目的:初步探讨紫草素对大鼠急性脊髓损伤(spinal cord injury,SCI)后神经功能恢复的影响及作用机制。方法:将96只Sprague-Dawley(SD)雄性大鼠分为4组:假手术组,即A组;假手术+紫草素组,即B组;脊髓损伤+二甲基亚砜(dimethyl sulfoxide,DMSO)组,即C组;脊髓损伤+紫草素组,即D组;每组24只。C、D组采用钳夹法制作大鼠急性SCI 模型。所有大鼠硬膜下置管,A 组不给药,B组和D组造模后30 min 经导管注射紫草素100 mg·kg^-1,C组注射等量 DMSO,每日1次,至取材时间点。各组分别于造模后6、12 h和3 d 每组取8只大鼠,行 Basso-Beattie-Bresnahan(BBB)评分及造模后1、3、7、14、21 d行斜板实验,再处死动物取脊髓组织。造模后1 h 每组大鼠腹腔注射碘化丙啶(propidine iodide,PI)1 mg·kg^-1,术后24 h取材检测脊髓组织 PI 红染细胞数;24 h 时取材采用苏木素-伊红(haematoxylin eosin,HE)染色观察脊髓损伤情况,尼氏(Nissl)染色观察神经元存活数量,使用Western-blot技术检测 B细胞淋巴瘤-2(B cell lymphoma-2,Bcl-2)蛋白及凋亡相关蛋白受体相互作用蛋白激酶1(receptor-interacting protein kinase 1,RIPK1)的表达水平。结果:造模后A组和B组各时间点的 BBB 评分均正常,C、D组各时间点均低于A、B组,D组造模后12 h和3 d的 BBB 评分高于同时间点C组(P<0.05)。造模后12 h,D组PI 红染细胞较C 组明显减少,神经元崩解减轻(P<0.05)。造模后24 h,A 组和 B 组脊髓组织 HE 和 Nissl 染色正常,D 组脊髓组织损伤程度和存活神经元数量均优于 C 组(P<0.05)。Bcl-2、RIPK1蛋白在A 组、B 组表达很低; RIPK1 在C组表达明显增高,在D组表达明显下降,差异有统计学意义(P<0.05);Bcl-2蛋白在D 组表达高于C 组(P<0.05)。结论:紫草素可减轻大鼠急性SCI后的病理变化,改善行为学评分,促进脊髓神经功能恢复。其具体机制可能与抑制TNFR/RIPK1信号通路介导的坏死性凋亡有关。     

大剂量甲基强的松龙对大鼠急性脊髓损伤后神经细胞Bcl-2表达及细胞凋亡的影响

目的：观察大剂量甲基强的松龙（MP）治疗对大鼠急性脊髓损伤（ASCI）后神经细胞凋亡及凋亡基因Bcl-2的影响。方法：选取48只雌性SD大鼠随机等分为2组,对照组与治疗组,按Nystrom法制备大鼠急性脊髓损伤模型。治疗组伤后30min经腹膜腔注入MP30mg／kg,以后每小时腹膜腔注入MP5．4mg／kg,维持24h;对照组应用生理盐水替代MP,处理方法同治疗组。两组分别于伤后4、8h及1、3、7、14d灌注固定后取材。免疫组织化学检测损伤段脊髓内Bcl-2蛋白表达,TUNEL检测细胞凋亡,染色结果应用图像分析仪进行半定量分析。结果：大鼠ASCI后4h即可见脊髓内TUNEL阳性细胞,8h表达达高峰,此后表达量逐渐下降,14d时仍可见少量阳性细胞。凋亡相关蛋白Bcl-2在伤后4h即可见表达,伤后1d达高峰,伤后14d仍有表达,与对照组相比,治疗组伤后8h、1d和3d时凋亡细胞数减少有统计学意义,伤后8h和1d Bcl-2蛋白表达增高有统计学意义。结论：大剂量甲基强的松龙治疗可抑制大鼠ASCI后神经细胞凋亡,并增加凋亡相关蛋白Bcl-2的表达：     

Effects of mild and moderate hypothermia on apoptosis in neuronal PC12 cells

Background. There is still a possibility that mild hypothermictherapy may be useful as a neuroprotective tool during the intraoperativeperiod, although the mechanism of cerebral protection by mildhypothermia is not well understood. We hypothesized that mildhypothermia may be protective against cerebral ischaemia byinhibiting post-ischaemia apoptosis. In this study, we usedserum-deprived PC12 cells as the neuronal apoptotic model andexamined the direct effects of mild and moderate hypothermia. Methods. Apoptosis was induced by depriving the cell culturemedium of serum, which is one of the most representative methodsto induce apoptosis, but not necrosis, in PC12 cells. Effectsof mild (35 and 33°C) and moderate (31 and 29°C) hypothermiaon apoptosis were evaluated. Cytotoxicity (lactate dehydogenaseleakage) and the percentage of apoptotic cells (calculated byflow cytometry with propidium iodide) were evaluated 4 daysafter induction of apoptosis. As a control, cells without inductionof apoptosis were incubated under the same conditions as theapoptosis group. Results. Without induction at 37°C, cytotoxicity and thepercentage of apoptotic cells were over 60 and 90%, respectively.At each temperature examined below 35°C, significant decreasesin cytotoxicity and the percentage of apoptotic cells were observed.Mean cytotoxicity at 31 and 29°C was 50.2 (SD 4.2)% and47.9 (4.4)%, respectively. The percentage of apoptotic cellsat 31 and 29°C was 42.5 (7.4)% and 36.5 (7.3)%, respectively.In the control group, cytotoxicity and the percentage of apoptoticcells were significantly higher at 29°C than at 37°C. Conclusions. Mild and moderate hypothermia (29–35°C)inhibited apoptosis, although hypothermia below 30°C mayinduce apoptosis in intact cells. Br J Anaesth 2002; 89: 301–5     

Posttraumatic hypothermia reduces polymorphonuclear leukocyte accumulation following spinal cord injury in rats

The present study addresses the effects of moderate posttraumatic hypothermia (32 degrees C) on the temporal and regional profile of polymorphonuclear leukocyte (PMNL) accumulation after traumatic spinal cord injury (SCI). We hypothesized that posttraumatic hypothermia would reduce the degree of inflammation by reducing PMNL infiltration. Rats underwent moderate spinal cord injury at T10 using the NYU impactor device. In the first study, the temporal profile of myeloperoxidase (MPO) activity (a marker of neutrophil accumulation) under normothermic (37 degrees C) conditions was determined. The animals were allowed to survive for 3 or 24 h, or 3 or 7 days after SCI. Spinal cords were dissected into five segments rostral and caudal to the injury site. Additional animals were studied for the immunocytochemical visualization of MPO. In the second study, rats were sacrificed at 24 h after a monitoring period of normothermia (36.5 degrees C/3 h) or hypothermia (32.4 degrees C/3 h) with their controls. In the time course studies, MPO enzymatic activity was significantly increased at 3 and 24 h within the traumatized T10 segment compared to controls. MPO activity was also increased at 3 h within the rostral T8 and T9 segments and caudal T11 and T12 segments compared to controls. At 24 h after trauma, MPO activity remained elevated within both the rostral and caudal segments compared to control. By 3 days, the levels of MPO activity were reduced compared to the 24-h values but remained significantly different from control. Neutrophils that exhibited MPO immunoreactivity were seen at 6 and 24 h, with a higher number at 3 days. PMNLs were located within the white and gray matter of the lesion and both rostral and caudal to the injury site. Posttraumatic hypothermia reduced MPO activity at 24 h in the injured spinal cord segment, compared to normothermic values. The results of this study indicate that a potential mechanism by which hypothermia improves outcome following SCI is by attenuating posttraumatic inflammation.     

Neuroprotective assessment of prolonged local hypothermia post contusive spinal cord injury in rodent model

Background Context

Although general hypothermia is recognized as a clinically applicable neuroprotective intervention, acute moderate local hypothermia post contusive spinal cord injury (SCI) is being considered a more effective approach. Previously, we have investigated the feasibility and safety of inducing prolonged local hypothermia in the central nervous system of a rodent model.

Inhibiting effect of moderate hypothermia on cell apoptosis after diffuse brain injury in rats

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大鼠脊髓损伤后巢蛋白在脊髓组织中的表达

目的探讨大鼠脊髓损伤后巢蛋白(nestin)的表达规律及其意义。方法30只Wister成年大鼠,随机分为正常对照组(A组)、损伤组(B组)。采用Allen打击模型(25g·cm),在T10段造成急性脊髓损伤,于损伤后1d、3d、1周、4周、8周进行取材,对距离损伤中心5mm处脊髓进行nestin免疫组化检测。应用图像分析软件进行nestin阳性区域面积侧算。结果A组脊髓室管膜细胞只可见极少数细胞胞浆内nestin表达,白质中几乎无表达。B组中nestin于损伤后24h表达于室管膜以及软膜,灰质和白质亦有少量表达,1周达到高峰(P<0.05),4周明显下降,8周时很少或几乎无表达。结论脊髓组织的许多部位可能存在具有分化和更新潜能的祖细胞,脊髓损伤后这些细胞被激活,在功能恢复中可能发挥着重要的作用。