硬膜外腔植入髓核对大鼠脊髓背根神经节SP和CGRP表达的影响

目的 观察硬膜外腔植入异体髓核对大鼠L6-S1,脊髓背根神经节细胞SP和CGRP表达的影响,以期为椎间盘源性疼痛发病机制提供细胞生物学基础.方法 18只雄性SD大鼠(体重260-280g)随机分为三组:脂肪组、髓核组、假手术组,每组n=6.另外3只雄性SD大鼠用来提供异体脂肪和髓核.术后第30d取L4-L6脊髓背根神经节和脊髓背角,采用免疫组织化学染色方法 观察髓核对脊髓背角和背根神经节细胞肽类神经递质SP和CGRP表达的影响.结果 术后30d脂肪组大鼠与假手术组相比,脊髓背角和背根神经节细胞SP和CGRP表达没有显著性差异(P>0.05);髓核组与脂肪组和假手术组相比脊髓背角和背根神经节细胞SP和CGRP表达显著增加(P<0.05).结论 硬膜外腔植入异体髓核可引起脊髓背根神经节细胞SP和CGRP表达增加.     

FasL在家兔退变髓核组织中的表达及其与白细胞介素-6和肿瘤坏死因子-α的相关性

目的 观察生理解剖学屏障与FasL的分子生物学效应之间的关系,探讨椎间盘退变的发病机制.方法 采用18规格的皮肤穿刺针穿刺家兔纤维环,在术后的3、6、10周收集正常及穿刺后的椎间盘组织,免疫组织化学染色观察FasL及白细胞介素(IL)-6和肿瘤坏死因子(TNF)-α等炎性因子的表达.结果 正常髓核组织中可见少许髓核细胞质中FasL呈弱阳性染色(8.7%),实验组髓核细胞质则呈强阳性染色(41.6%、48.8%、46.4%).FasL阳性细胞百分比在正常组与各实验组之间的两两比较,差异有统计学意义(P<0.01).实验组髓核细胞FasL阳性表达百分比与IL-6及TNF-α阳性表达百分比之间显著相关(r=0.424,P<0.05及r=0.527,P<0.01).结论 FasL与理解剖学屏障的共同作用,可能是使髓核组织产生免免效应的重要因素.当生理解剖学屏障受到损伤后(如穿刺纤维环),FasL、IL-6及TNF-α的表达程度增强,FasL所介导的免疫炎性反应是引起椎间盘退变的重要机制之一.     

siRNA转染对大鼠髓核细胞TRAIL表达和细胞行为的影响

[目的]探讨siRNA转染对大鼠髓核细胞TRAIL表达和细胞行为的影响。[方法]采用弯曲鼠尾法建立椎间盘退变模型。处死动物。取退变椎间盘组织分离培养髓核细胞。P1髓核细胞分为4组,分别为空白对照组、TRAIL-siRNA转染组(siTRAIL组)、TNF-α处理组(TNF-α组)和TNF-α处理+TRAIL-siRNA转染组(TNF-α+siTRAIL组)。采用MTT法检测P1髓核细胞增殖,流式细胞仪检测细胞凋亡,Western blot法检测髓核细胞Caspase-3的活性和表达。[结果]相较于空白对照细胞,TRAIL siRNA转染对细胞增殖、凋亡、Caspase-3的表达无明显影响(P0.05);TNF-α处理引发髓核细胞增殖显著下降(P0.05),而凋亡率显著升高(P0.05),Caspase-3的表达显著升高(P0.05)。TNF-α处理后再用TRAIL-siRNA转染可显著逆转TNF-α对细胞增殖、凋亡和Caspase-3表达的影响(P0.05)。[结论] TRAIL siRNA转染可沉默TRAIL表达,从而逆转TNF-α诱导大鼠髓核细胞增殖抑制、细胞凋亡和Caspase-3表达。     

整合素在人退变椎间盘髓核组织中的表达及意义

目的:观察整合素α1、α5、αv、β1、β3亚基在人退变椎间盘中的表达情况;探讨其在椎间盘退变中的意义.方法:术中收集人椎间盘髓核标本28个;其中6个来自6例脊柱骨折患者;设为对照组(n=6);22个来自20例椎间盘突出症患者;突出10个(突出组;n=10);脱出12个(脱出组;n=12).应用逆转录聚合酶链式反应(RT-PCR)和免疫沉淀技术测定整合素α1、α5、αv、β1、β3和整合素的配体——胶原蛋白(Ⅰ和Ⅱ型)、纤维结合蛋白在三组椎间盘髓核内的表达情况.结果:整合素α1、α5、αv、α1、α3在三组椎问盘髓核内都有表达;整合素α5在脱出组和突出组的表达分别是正常组的2.2倍和1.5倍;整合素β1在脱出组和突出组的表达分别是正常组的2.5倍和1.6倍;纤维结合蛋白的表达同样有升高的趋势.整合素α1、αv、β3在三组内的表达无统计学差异.结论:在退变的椎间盘髓核内整合素α5和β1亚基的表达增加;可能与椎间盘退变相关.     

促炎因子与抗炎因子在突出腰椎间盘组织中的表达及其意义

目的观察促炎因子白介素(IL)-6、肿瘤坏死因子(TNF)-α及抗炎因子白介素(IL)-4在退变椎间盘组织内的表达,并探讨其意义。方法收集30例单节段椎间盘突出症患者及10例经前路松解手术的特发性脊柱侧弯患者的髓核组织,术前患者临床症状严重程度均予Oswestry功能障碍指数(ODI)评定,23例行MRI检查的患者,根据Schneiderman分级评定椎间盘退变程度,术后应用酶联免疫吸附测定法(ELISA)测定髓核组织中IL-6、TNF-α和IL-4的含量。结果退变髓核中IL-6的含量(11.2±7.5)ng/L较对照组(6.4±0.8)ng/L高(P<0.01)、TNF-α的含量(186.8±86.0)ng/L亦较对照组(122.3±23.5)ng/L高(P<0.05);IL-4的表达仅存在于TNF-α表达较高的髓核组织中;IL-6及TNF-α的同时表达与ODI评分高低正相关(IL-6:B=0.481,β=0.229,P<0.05;TNF-α:B=6.945E-2,β=0.522,P<0.01);椎间盘退变MRI分级与促炎因子和抗炎因子的高低无明显相关。结论促炎因子TNF-α与IL-6的表达增高为椎间盘退变的重要原因,亦为临床症状加重的重要原因之一;促炎因子与抗炎因子表达的不平衡亦可能为椎间盘退变进展的重要因素。     

外源性肿瘤坏死因子-α诱发兔椎间盘退变中β-catenin蛋白的表达及意义

目的 通过外源性肿瘤坏死因子(TNF)-α注射构建兔椎间盘退变动物模型,探讨该模型中β-catenin蛋白的表达及意义和炎性细胞因子在促进腰椎间盘退变过程中Wnt/β-catenin信号通路的作用.方法 选取12只健康成年日本白兔,雌雄随机,体质量2.5～3.0kg.手术暴露L2～5 3个间隙共36个椎间盘.随机分为4组,分别注入生理盐水、TNF-α 5 ng、TNF-α 10ng、TNF-α 20 ng,于术后第8周统一处死,取椎间盘髓核组织作苏木素-伊红(HE)-番红O染色病理切片进行形态学观察;各组分别随机选取4个椎间盘髓核组织标本,采用蛋白印迹法(Western blot)测定β-catenin蛋白含量并比较各组间差异.结果 HE-番红O染色病理切片显示,在5、10、20 ng组椎间盘组织中髓核细胞数量减少,正常网状结构破坏,细胞形态发生改变,出现肥大空泡样软骨细胞,组织基质蛋白聚糖含量明显降低,番红O淡染,生理盐水对照组椎间盘形态基本正常,无退变发生.蛋白印迹结果显示β-catenin蛋白含量在注射TNF-α组明显增加,各组吸光度比值分别为:0.142±0.036、0.351±0.041、0.472±0.052和0.710±0.063,组间差异有统计学意义(P＜0.05)且与TNF-α浓度相关.结论 通过外源性TNF-α盘内注射能够成功构建兔椎间盘退变动物模型,且退变程度与TNF-α呈浓度依赖性;在退变模型髓核组织中β-catenin蛋白含量增高且与TNF-α浓度正相关,提示炎症细胞因子触发了Wnt/β-catenin信号通路,在椎间盘退变过程中可能发挥了重要作用.     

舒筋祛痹汤对腰椎间盘突出症大鼠PLA2活性、IL-6、TNF-α水平和椎间盘退变的影响

目的探究舒筋祛痹汤对腰椎间盘突出症(LDH)大鼠磷脂酶A2(PLA2)活性、白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)水平及椎间盘退变的影响。方法将60只SD雄性大鼠随机分为正常组、西医组、中医组各20只,除正常组大鼠正常环境下继续饲养以外,西医组、中医组建立LDH模型,并分别给予西药双氯芬酸钠肠溶片、中药舒筋祛痹汤连续灌胃给药14 d。于制模后3、7、14d分别取出移植髓核观察移植髓核组织内PLA2活性,并于断头处死大鼠后取血测定血清IL-6、TNF-α浓度,取L5神经根组织,常规脱蜡、HE染色、脱水、封片后观察病理改变。结果制模成功经大鼠灌胃后第3天,中药组、西药组大鼠髓核组织中PLA2活性达到最高,均显著高于正常组(P0.05);此时中药组髓核组织中PLA2活性略高于西药组,但差异无显著性(P0.05)。第7、14天中药组、西药组髓核组织中的PLA2活性均显著较第3天降低(P0.05),且第7、14天中药组髓核组织中PLA2活性均略低于西药组,但差异无显著性(P0.05)。制模成功经大鼠灌胃后第14天西药组、中药组血清IL-6、TNF-α浓度略高于正常组,但差异无显著性(P0.05);且中药组血清IL-6、TNF-α浓度略低于西药组,但差异无显著性(P0.05)。中药组大鼠神经根髓鞘、轴突及雪旺细胞病理变化较西药组改善明显。结论舒筋祛痹汤可降低LDH大鼠突出髓核组织PLA2活性及血清IL-6、TNF-α浓度,抑制炎症介质合成,从而起到与抗炎镇痛类西药类似效果,对延缓椎间盘退变有重要作用。     

破裂型椎间盘突出重吸收过程中P38MAPK信号通路的作用

目的 :构建大鼠自体尾椎破裂型椎间盘突出冲吸收动物模型,探讨P38丝裂原活化蛋白激酶(P38 mitogen-activated protein kinases,P38MAPK)信号通路在破裂型椎间盘突出重吸收中的作用。方法 :将40只3月龄SD大鼠随机分为对照组和实验组,每组20只。采用刺破大鼠自体尾椎椎间盘,包埋至L4-5背部肌肉的方法制作破裂型椎间盘突出重吸收模型。实验组从造模至取材之日予腹腔注射P38MAPK特异性阻断剂SB203580;对照组予腹腔注射生理盐水,分别在造模1周和4周后处死并取出包埋的椎间盘,电子天平称重。计算1周末和4周末椎间盘减少质量,镜下观察椎间盘形态退变情况。Real Time PCR法检测P38MAPK、肿瘤坏死因子α(tumour necrosis factor-α,TNF-α)、白细胞介素1β(interleukin-1β,IL-1β)、基质金属蛋白酶3(matrix metalloproteinase-3,MMP-3)、基质金属蛋白酶9(matrix metalloproteinase-9,MMP-9)的m RNA表达。Western Blot法检测TNF-α、IL-1β、MMP-3、MMP-9及磷酸化P38丝裂原活化蛋白激酶(phosphorylated p38mitogen-activated protein kinase,p-p38MAPK)的蛋白表达。结果 :实验组1周时椎间盘质量减小0.47±2.90mg,4周时减少1.11±3.05mg,两组之间无统计学差异(P0.05),对照组1周时椎间盘质量减小4.15±1.84mg,4周时减少10.56±3.29mg,两组之间存在统计学差异(P0.05)。镜下可见,实验组4周时与1周时相比,组织形态无明显退变,对照组4周时与1周时相比,组织形态出现明显退变。Real Time PCR检测,1周时,实验组椎间盘髓核组织中TNF-α、p38MAPK、MMP-3、MMP-9的m RNA表达低于对照组(P0.05);4周时,实验组TNF-α、IL-1β、p38MAPK、MMP-3的m RNA表达低于对照组(P0.05)。Western Blot法检测,4周时,实验组椎间盘组织中TNF-α、P38MAPK、P-p38MAPK、MMP-3的蛋白表达低于对照组(P0.05);对照组4周时椎间盘组织中TNF-α、IL-1β、P-p38MAPK的蛋白表达均高于1周时(P0.05)。对照组髓核组织中P-p38MAPK与MMP-3、IL-1β、TNF-α的蛋白表达呈正相关(0r1,P0.05)。结论 :P38阻断剂可能通过抑制髓核组织中P38MAPK的磷酸化,降低TNF-α、IL-1β、MMP-3、MMP-9的m RNA和蛋白体表达,从而抑制突出椎髓核组织重吸收。     

雌激素α、β受体在大鼠椎间盘组织中的免疫组织化学定位

[目的]探讨雌激素α、β受体(ERα、ERβ)在大鼠椎间盘组织的定位和分布.进一步探讨ER与椎间盘退变的关系,对早期预防和治疗椎间盘退变提供一定的理论依据.[方法]用免疫组织化学染色法(Elivison二步法)检测大鼠关节软骨,椎体终板及椎间盘组织中ER-α,ER-β的表达及分布情况.[结果]免疫组织化学染色见ER-α,ER-β在椎体骨组织中表达明显,在终板软骨组织表达较为明显,在髓核组织中均有表达,在纤维环中未见表达.[结论]在大鼠的髓核组织中的髓核细胞(类软骨细胞)中存在ER.     

大鼠尾椎椎间盘退变静态压力模型的构建

目的采用静态压力构建稳定的大鼠尾椎椎间盘退变模型。方法将40只12周龄大鼠随机分为静态压力组和针刺组,每组20只。静态压力组:在尾椎C_(4~7)椎体上安装静态压力环形外固定支架,压缩的4根弹簧施加的压强均为10 kPa,维持8周。针刺组:采用16 G针头刺入尾椎C_4/C_5/C_6/C_7椎间盘,限制损伤深度5 mm、朝向椎间盘中心,损伤后留置10 s。分别于术后8周进行组织病理学切片观察,采用秩和检验比较2组Thompson椎间盘退变病理分级。结果对2组大鼠尾椎共120个椎间盘髓核组织标本进行病理分级,统计结果显示静态压力组退变级别明显高于针刺组,差异有统计学意义(P0.05)。结论采用静态压力构建的椎间盘退变模型稳定可靠,较传统针刺模型具有优势,可为临床椎间盘退变研究提供可靠的动物模型。     

TNF-α抑制剂对破裂型腰椎间盘突出重吸收影响的实验研究

目的 研究TNF-α抑制剂(益赛普)对破裂型腰椎间盘突出重吸收的影响作用.方法 将42只雄性SD大鼠在适应性喂养2周后随机分为空白组和药物组.空白组分两种模型:随机分为模型组Ⅰ(椎间盘不刺破组)、模型组Ⅱ(椎间盘刺破组);药物组(TNF-α抑制剂组)给以益赛普注射.动物造模成功后给药4周后处死,所取得的大鼠椎间盘进行T...     

人体退变椎间盘中PDGF-A、PDGFR-α的表达及生物学意义

目的 观察人体退变椎间盘组织中血小板源性生长因子-A(PDGF-A)、血小板源性生长因子受体-α(PDGFR-α)的表达,探讨其生物学意义.方法 免疫组化(S-P)法分别检测PDGF-A、PDGFR-α、增殖细胞核抗原(PCNA)在正常对照组(A组,n=17)、退变椎间盘组(B组,n=51)中的表达;TUNEL法检测两...     

Both expression of cytokines and posterior annulus fibrosus rupture are essential for pain behavior changes induced by degenerative intervertebral disc: An experimental study in rats

The aim of this study was to analyze the relationship between intervertebral disc degeneration and low back pain (LBP). Rat L4/5 disc degeneration model was established by annular puncture using a 0.4 mm needle anteriorly or posteriorly. In both anterior and posterior puncture models, magnetic resonance imaging (MRI) and histological analyses revealed marked disc degeneration 2 weeks after puncture. Cytokine expression was up‐regulated in different level in nucleus pulposus (NP) from 3 days after puncture. Pain behavioral tests indicated that the anterior disc puncture did not induce pain behavior changes, whereas the posterior disc puncture resulted in mechanical allodynia from 1 day to 21 days after injury. Besides, cytokine expression was significantly increased in dorsal root ganglion (DRG) at 1 and 2 weeks after posterior puncture, but not after the anterior puncture. These findings indicate the NP of the degenerative disc expresses different levels of inflammatory cytokines, and posterior disc puncture produced mechanical allodynia. The expression phase of cytokines in the NP was accordance with mechanical hyperalgesia in the posterior disc puncture model. Both expression of cytokines and posterior annulus fibrosus (AF) rupture in degenerative intervertebral disc are essential for pain behavior changes. © 2013 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 32:262–272, 2014.     

Human nucleus pulposus cells react to IL-6: independent actions and amplification of response to IL-1 and TNF-α

STUDY DESIGN.: Human nucleus pulposus cells were activated with IL-6 plus IL-6 soluble receptor (sR) in the presence or absence of IL-1β or TNF-α. Cell production of factors modulating the anabolic/catabolic balance of the disc and proteoglycan synthesis were determined. OBJECTIVE.: To evaluate NP cell response to exogenous IL-6, and how IL-6 modulates IL-1 and TNF-α actions in these cells. SUMMARY OF BACKGROUND DATA.: Interleukin-6 (IL-6) is produced by cervical and lumbar herniated discs and is associated with neurological symptoms of intervertebral disc degeneration. It upregulates catabolic gene expression and downregulates matrix protein gene expression in chondrocytes. However, no studies have evaluated the effects of IL-6 on disc nucleus pulposus (NP) cells. METHODS.: NP cells from degenerated human discs were expanded in monolayer, maintained in alginate bead culture, and activated with IL-6 plus IL-6 soluble receptor (sR), in the presence or absence of IL-1β or TNF-α. Conditioned media was collected and analyzed for nitrite, PGE-2, TIMP-1, MMP-3, VEGF, and IL-8. Proteoglycan synthesis was assayed as S-sulfate incorporation normalized to DNA content and relative gene expression measured by rtPCR. RESULTS.: IL-6 + sR decreased collagen and aggrecan message, proteoglycan synthesis, and exacerbated the downregulation of proteoglycan synthesis effected by IL-1. PGE-2 synthesis was increased by IL-6 + sR, as was the induction of COX-2 mRNA. IL-6 + sR also enhanced IL-1 and TNF-α stimulated synthesis of PGE-2. IL-6 + sR induced MMP-3 approximately twofold and increased gene expression and synthesis in cells exposed to IL-1 and TNF-α. MMP-13 induction by TNF-α was also potentiated by IL-6 + sR. IL-6 + sR induced IL-6 gene expression and increased that stimulated by TNF-α fourfold. CONCLUSION.: The results suggest maneuvers to diminish IL-6 production in the disc could provide some protection against the adverse effects of IL-1 and TNF-α, thus, helping preserve disc composition, structure, and function.     

慢性软组织损害性疼痛外周不同组织中TNF-α表达的研究

目的 研究慢性软组织损害性疼痛患者不同外周组织中TNF-α的表达,探讨其致痛机制。方法 选择行手术治疗的软组织损害性疼痛患者18例作为实验组,腰椎间盘突出症患者16例为对照组,分别取腰部深筋膜、肌肉、骨表面软组织标本,检测各部位组织中TNF-α的表达并进行比较。结果 实验组中肌肉组织TNF-α的表达最高,与深筋膜和骨表面组织相比有显著差异（P〈0.05）,与对照组相比有显著差异（P〈0.05）,对照组各组织中TNF-α表达相比无差异。结论TNF-α在慢性软组织损害性疼痛中可能起重要作用,肌肉组织是疼痛的主要病灶部位。     

高迁移率族蛋白B1 mRNA在脓毒症大鼠脾脏中的表达

目的：探讨高迁移率族蛋白B1（HMGB1）mRNA在脓毒症大鼠外周免疫器官脾脏的表达规律及其与血清肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）的关系。方法：采用盲肠结扎穿孔（CLP）方法制备大鼠脓毒症模型。83只大鼠随机分为正常对照组（10只）、盲肠结扎穿孔组（38只）,盲肠结扎穿孔丙酮酸乙酯治疗组（35只）。分别于CLP术后4、12、24、48、72h或CLP术后丙酮酸乙酯治疗12、24、48、72h活杀动物,留取脾脏组织和血清标本,用半定量逆转录-聚合酶链式反应（RT-PCR）技术检测脾脏组织HMGB1mRNA的表达规律,用放射性免疫方法检测血清TNF-α和IL-6的浓度。结果：HMGB1mRNA在正常大鼠脾脏组织有轻度表达,CLP术后表达显著增强（P〈0.05）。CLP术后24h和72h分别出现两个高峰。丙酮酸乙酯液治疗可显著降低CLP术后大鼠脾脏组织HMGB1mRNA的表达（P〈0.05）。CLP术后大鼠血清TNF-α和IL-6浓度显著增高（P〈0.05）,丙酮酸乙酯治疗可显著降低CLP术后大鼠TNF-α和IL-6的浓度（P〈0.05）。结论：HMGB1在脓毒症大鼠外周免疫器官脾脏的表达显著增高,并与血清TNF-α和IL-6等炎症因子的增高有重要关系;HMGB1参与了失控性炎症反应的发展过程。     

Inflammatory cytokine and catabolic enzyme expression in a goat model of intervertebral disc degeneration

Intervertebral disc degeneration is implicated as a leading cause of low back pain. Persistent, local inflammation within the disc nucleus pulposus (NP) and annulus fibrosus (AF) is an important mediator of disc degeneration and negatively impacts the performance of therapeutic stem cells. There is a lack of validated large animal models of disc degeneration that recapitulate clinically relevant local inflammation. We recently described a goat model of disc degeneration in which increasing doses of chondroitinase ABC (ChABC) were used to reproducibly induce a spectrum of degenerative changes. The objective of this study was to extend the clinical relevance of this model by establishing whether these degenerative changes are associated with the local expression of inflammatory cytokines and catabolic enzymes. Degeneration was induced in goat lumbar discs using ChABC at different doses. After 12 weeks, degeneration severity was determined histologically and using quantitative magnetic resonance imaging (MRI). Expression levels of inflammatory cytokines (tumor necrosis factor-α [TNF-α], interleukin-1β [IL-1β], and IL-6) and catabolic enzymes (matrix metalloproteinases-1 [MMPs-1] and 13, and a disintegrin and metalloproteinase with thrombospondin type-1 motifs-4 [ADAMTS-4]) were assessed as the percentage of immunopositive cells in the NP and AF. With the exception of MMP-1, cytokine, and enzyme expression levels were significantly elevated in ChABC-treated discs in the NP and AF. Expression levels of TNF-α, IL1-β, and ADAMTS-4 were positively correlated with histological grade, while all cytokines and ADAMTS-4 were negatively correlated with MRI T2 and T1ρ scores. These results demonstrate that degenerate goat discs exhibit elevated expression of clinically relevant inflammatory mediators, and further validate this animal model as a platform for evaluating new therapeutic approaches for disc degeneration.     

Evaluation of behavior and expression of NaV1.7 in dorsal root ganglia after sciatic nerve compression and application of nucleus pulposus in rats

Purpose

The pathomechanisms of pain resulting from lumbar disc herniation have not been fully elucidated. Prostaglandins and cytokines generated at the inflammatory site produce associated pain; however, non-steroidal anti-inflammatory drugs and steroids are sometimes ineffective in patients. Tetrodotoxin-sensitive voltage-gated sodium (NaV) channels are related to sensory transmission in primary sensory nerves. The sodium channel NaV1.7 has emerged as an attractive analgesic target. The purpose of this study was to evaluate pain-related behavior and expression of NaV1.7 in dorsal root ganglia (DRG) after combined sciatic nerve compression and nucleus pulposus (NP) application in rats.

Methods

Rats were divided into three groups and underwent either sciatic nerve compression with NP for 2 s using forceps (n = 20), sham operation with neither compression nor NP (n = 20), or no operation (controls, n = 20). Mechanical hyperalgesia was measured every second day for three weeks using von Frey filaments. NaV1.7 expression in L5 DRG was examined 7 and 14 days after surgery using immunohistochemistry. The number of neurons immunoreactive for NaV1.7 was compared among the three groups.

Results

Mechanical hyperalgesia was found over the 14-day observation in the nerve compression plus NP application group, but not in the sham-operated or control groups (P < 0.05). NaV1.7 expression in L5 DRG was up-regulated in the nerve compression plus NP application group, compared with sham-operated and control rats (P < 0.01).

Conclusions

Our results indicate that nerve compression plus NP application produces pain-related behavior. We conclude that NaV1.7 expression in DRG neurons may play an important role in mediating pain from sciatic nerves after compression injury and exposure to NP.     

新型腹腔降温法对心肺复苏后兔肠黏膜损伤的影响

目的探讨心肺复苏后腹腔降温法对肠黏膜损伤的保护作用。方法 36只健康成年新西兰大白兔用交流电致颤的方式建立室颤模型,自主循环恢复后,模型动物随机分为常温治疗组(NT)、体表降温组(SC)和腹腔降温组(PC)。观察每组自主循环恢复(ROSC)后鼓膜温度和腹腔温度的变化,ROSC后12h处死动物,观察肠黏膜损伤情况和炎症因子TNF-α和VCAM-1的表达情况。结果每组12只动物,NT、SC和PC组各有9、10和9只动物CPR成功,ROSC后动物均需要行机械通气2～4h,各组分别有5、6和8只动物存活到实验结束。NT组的鼓膜、腹膜温度均维持在正常范围内,SC和PC两组的鼓膜温度达到目标温度的时间分别为(29±6.55)min和(62±8.27)min。维持亚低温阶段,SC组腹腔内温度和鼓膜温度维持在33℃～35℃,而PC组腹腔温度维持在31℃～34℃。PC组肠黏膜损伤评分为1.43±0.53,低于NT组的3.40±0.55(P0.01)和SC组的3.17±0.41(P0.05),而NT组和SC组之间差异不明显(P=0.30)。肠黏膜内TNF-α的表达NT组为(9.98±1.79)%,高于SC组的(5.87±1.43)%和PC组的(2.54±0.96)%,差异有统计学意义(P0.05);SC组和PC组之间差异有统计学意义(P0.05)。SC组肠黏膜内VCAM-1的表达为(5.92±1.06)%,PC组为(3.78±0.53)%,两组VCAM-1表达水平显著低于NT组(8.53±1.53)%,P分别小于0.01和0.05,PC组VCAM-1表达水平也显著低于SC组,P0.05。结论 CPR后腹腔降温法除能快速诱导亚低温外还能减轻ROSC后的肠黏膜损伤。