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兔椎间盘生理屏障损伤后髓核组织辅助性T细胞1/辅助性T细胞2平衡漂移状态的研究 被引量:2

Construction of the state of helper T cell 1/helper T cell 2 balance drift after physiological barrier injury of rabbit intervertebral disc
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摘要 目的探讨兔椎间盘生理屏障损伤后辅助性T细胞1(Thl)/辅助性T细胞2(Th2)平衡漂移状态。方法采用纤维环穿刺构建兔椎间盘退变的动物模型,在术后1、3d、1、3周采集外周静脉血,采用双抗夹心酶联免疫吸附测定(ELISA)方法,分别检测血清中Th1、Th2型细胞因子水平[肿瘤坏死因子(TNF)-α、干扰素(IFN)-1、白细胞介素(IL)-10及IL-4]。结果造模后的1、3d、1、3周兔血清中TNF-α含量分别为(150.531±56.74)、(83.833±37.434)、(90.990±3.554)、(87.950±13.289)ng/L;IFN-γ含量分别为(99.263±18.421)、(125.427±9.156)、(180.368±18.293)、(165.531±12.548)ng/L,明显高于造模前(P〈0.05),术后各个时间点模型组血清中TNF-α与IFN-γ含量高于假手术组与正常组(P〈0.05)。造模后的1、3d、1、3周兔血清中IL-10含量分别为(33.947±3.164)、(27.928±0.493)、(29.992±4.33)、(30.0254-2.339)ng/L;IL4含量分别为(34.517±3.032)、(35.056±1.882)、(35.983±2.369)、(32.549±5.086)ng/L,与术前比较未见明显增高(P〉0.05)。术后各个时间点模型组血清中IL-10与IL-4含量与假手术组及正常组比较差异无统计学意义(P〉0.05)。结论生理屏障损伤后椎间盘发生退变的机制与Th1优势状态有关。 Objective To explore the state of helper T cell 1 ( Thl ) / helper T cell 2 (Th2) bal- ance drift after physiological barrier injury of rabbit intervertebral disc. Methods A rabbit model of inter- vertebral disc degeneration was established by anular puncture. Peripheral venous blood was collected at 1st, 3rd, 7th, and 21st day after surgery. Serum levels of Thl/Th2 cytokiues [ tumor necrosis factor (TNF) - α, interferon (IFN) - γ, interleukin (IL) - 10 and IL - 4 ] were determined by ELISA. Re- sults At 1 st, 3rd, 7th, and 21st day after surgery, the serum TNF - ct level was ( 150. 531 ± 56. 74), ( 83. 833 ± 37. 434), (90. 990 ± 3. 554) and ( 87. 950 ± 13.289 ) ng,/L respectively, and serum IFN -γ level was (99. 263 ± 18. 421 ), ( 125. 427 ±9. 156), ( 180. 368 ± 18. 293) and ( 165. 531 ± 12. 548) ng/L respec- tively, which were markedly increased after modeling (P 〈0.05 or P 〈0. 01 ). At 1st, 3rd, 7th, and 21st day after modeling, the serum IL - 10 level was (33. 947 ±3. 164), (27.928 ±0. 493), (29. 992 ±4. 33) and (30. 025 ±2.339) ng/L, and serum IL -4 level was (34.517 ±3.032), (35.056 ± 1.882), (35.983 ± 2. 369) and ( 32. 549 ± 5. 086) ng/L respectively. As compared with preoperation, the serum IL - 10 and IL -4 levels in three groups after operation were not significantly increased (P 〉 0. 05 ). There was no significant difference in serum IL - 10 and IL - 4 levels among three groups ( P 〉 0. 05 ). Conclu- sion Mechanism of intervertebral disc degeneration after physiological barrier injury may be related to Thl state.
出处 《中华实验外科杂志》 CAS CSCD 北大核心 2016年第3期727-729,共3页 Chinese Journal of Experimental Surgery
基金 浙江省自然科学基金(LY12H06004) 国家自然科学基金(81202711)
关键词 椎间盘 生理屏障损伤 辅助性T细胞1/辅助性T细胞2平衡漂移 Intervertebral disc Physiological barrier injury Rabbit Helper T cell t/helper T cell 2 balance drift
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参考文献10

  • 1Olmarker K,Blomquist J,Stromberg J,et al.Inflammatogenic proper- ties of nucleus pulposus[J].Spine,1995 ,20(6):665-669.
  • 2Satoh K,Konno S,Nishiyama K,et al.Presence and distribution of an- tigen-antibody complexes in the herniated nucleus pulposus [J].Spine,1999,24(19):1980-1984.
  • 3Burke JG,Watson RW,Mclormack D,et al.Intervertebral discs which cause low pain back secrete high levels of proinflammatory mediators [J].J Bone Joint Surg Br,2002 ,84(2):196-203.
  • 4Aoki Y,Rydevik B,Kikuchi S,et al.Local application of disc-related cytokines on spinal nerve roots [J].Spine,200227(15):1614-1617.
  • 5Kato T,Haro H,Komon H ,et al.Sequential dynamics of inflammatory cytokine,angiogensis inducing factor and matrix degrading enzymes during spontaneous resportion of the heriated disc [J].Orthop Re- search ,2004,22(4):885-900.
  • 6Yoshihara Y,Nakamura H,Kikuchi T,et al.Expression of monocyte chemoattractant protein -1 in primary cultures of rabbit interveirtebral disc cells[J].Orthop Res,2002 ,20(6):1298-1304.
  • 7Elenkov LJ.Glucocorticoids and the Th1/Th2 balance[J].Ann N Y Acad Sci,2004,1024:138-146.
  • 8Kidd P.Th1/Th2 balance:the hypothesis,its limitations,and implica- tions for health and disease [J].Altem Med Rev,2003 ,8(3):223-246.
  • 9王靖,唐天驷,姚啸生,李涛,史勇.纤维环穿刺诱导椎间盘退变动物模型的实验研究[J].中国脊柱脊髓杂志,2006,16(4):284-287. 被引量:26
  • 10王靖,唐天驷,滕红林,黄卡特.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[J].中华实验外科杂志,2010,27(1):114-115. 被引量:5

二级参考文献20

  • 1黄东生,丁悦,叶伟,苏培强,刘尚礼,梁蔚文.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[J].中华实验外科杂志,2006,23(1):86-87. 被引量:38
  • 2王靖,唐天驷,姚啸生,李涛,史勇.纤维环穿刺诱导椎间盘退变动物模型的实验研究[J].中国脊柱脊髓杂志,2006,16(4):284-287. 被引量:26
  • 3李旭,侯筱魁,李惠武,汤亭亭,郭刚,裴国献.“穿刺抽取髓核”诱导腰椎间盘退变的时间相关性评估[J].中华实验外科杂志,2007,24(6):672-674. 被引量:8
  • 4Nagata S.A role for CD95 ligand in preventing graft rejection.Nature,1995,1377:630-632.
  • 5Nagata S.Apoptosis by death factor.Cell,1997,88:355-365.
  • 6Griffith TS,Brunner T,Fletcher SM,et al.FasL-induced apoptosis as a mechanism of immune privilege.Science,1995,1270:1189-1192.
  • 7Bellgrau D,Gold D,Selawry H,et al.A role for CD95 ligand in preventing graft rejection.Nature,1995,1377:630-632.
  • 8Bechmann I,Mor G,Nilsen J,et al.FasL (CD95L,ApolL) is expressed in the normal rat and human brain:evidence for the existence of an immunological brain barrier.Glia,1999,27:62-74.
  • 9Park JB,Chang H,Kim KW.Expression of Fas ligand and apoptosis of disc cells in herniated lumbar disc tissue.Spine,2001,26:618-621.
  • 10Gruber HE,Johnson T,Norton HJ,et al.The sand rat model for disc degeneration:radiologic characterization of age-related changes:cross-sectional and prospective analyses [J].Spine,2002,27 (3):230-234.

共引文献29

同被引文献32

  • 1Smith M, Davis MA, Stano M, et aI.Aging baby boomers and the rising cost of chronic back pain: Secular trend analysis of longitudinal Medical Expenditures Panel Survey data for years 2000 to 2007.J Manipulative Physiol Ther.2013;36(1):2-11.
  • 2Son S, Kim WK, Lee SC et al.A comparison of the clinica outcomes of decompression alone and fusion in elderly patients with two-level or more lumbar spinal stenosis. J Korean Neurosurg Soc.2013;53(1 ):19-25.
  • 3Takahashi N, Kikuchi S, Shubayev VI, et al. TNF-alpha and phosphonjlation of ERK in DRG and spinal cord: insights into mechanisms of sciatica. Spine. 2006;31 (5) 523-529.
  • 4Kaymaz M,Borcek AO,Emmez H,et aI.Effectiveness of single posterior decompressive laminectomy in symptomatic lumbar spinal stenosis: a retrospective study Turk Neurosurg. 2012;22(4):430-434.
  • 5Ozaktay AC, Kallakuri S, Takebayashi T, et al. Effects of interleukin-1 beta, interleukin-6, and tumor necrosis factor on sensitivity of dorsal root ganglion and peripheral receptive fields in rats. Eur Spine J. 2006; 15(10):1529-1537.
  • 6William CW, Jamie B, Thomas JG, et al. Degenerative lumbar spinal stenosis : an evidence-based clinical guide line for the diagnosis and treatment of degenerative lumbar spinalstenosis. Spine. 2008;2: 305-310.
  • 7Nakamura T, Okada T, Endo M, et al. Angiopoietin-like protein 2 induced by mechanical stress accelerates degeneration and hypertrophy of the ligamentum flavum in lumbar spinal canal stenosis. PLoS One. 2014;9(1 ):e85542.
  • 8Podichetty VK. The aging spine: the role of inflammatory mediators in intervertebral disc degeneration. Cell Mol Biol (Noisy-le-grand). 2007;53(5):4-18.
  • 9Gronbald M, Virri J, Tolonen J, et al. A Controlled immunohistochemical study of inflammatory cells in disc herniation tissue. Spine. 1994;19:2744.
  • 10Gruber-Schoffnegger D, Drdla-Schutting R, H6nigsperger C,et al. Induction of thermal hyperalgesia and synaptic long-term potentiation in the spinal cord lamina I by TNF-aand IL-113 is mediated by glial cells. J Neu rosci. 2013;33(15):6540-6551.

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