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一氧化氮对兔纤维环细胞线粒体功能的影响及机制研究 被引量:2

Regulating Effect and Mechanism of Nitric Oxide on Mitochondrial Function of Rabbit Annulus Fibrosus Cells
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摘要 目的:研究一氧化氮(NO)对兔纤维环细胞线粒体功能的影响及其与纤维环细胞生物学行为的相关性。方法:平板培养的兔腰椎间盘纤维环细胞,将其分为6组加入不同剂量的NO供体硝普钠(SNP)及烟酰胺:A组,不加入药物;B组,10μmol/LSNP;C组,100μmol/LSNP;D组200μmol/LSNP;E组,100μmol/LSNP和0.05mg/ml烟酰胺;F组,100μmol/LSNP和0.5mg/ml烟酰胺。作用72h后检测细胞增殖活力、细胞内ATP含量、细胞内一氧化氮合酶(NOS)活性以及线粒体膜电位。结果:兔纤维环细胞经不同浓度的SNP作用72h后,细胞内NOS量随SNP加大而增加、ATP量则随着减小,和对照组比较差异有统计学意义(P<0.05);SNP组可引起纤维环细胞膜电位下降,烟酰胺组可减轻因SNP引起的膜电位下降(P<0.05);与SNP组比较烟酰胺组呈浓度依赖性促进纤维环细胞增殖(P<0.05)及改善纤维环细胞的增殖能力,两组间比较差异有统计学意义(P<0.05)。结论:过量的NO可损害兔纤维环细胞的线粒体代谢功能,通过抑制NO的合成以及保护椎间盘细胞线粒体的功能,有助于预防椎间盘退变。 Objective:To investigate the regulatory effect of nitric oxide (NO) on mitochondrial function and biological behavior of rabbit annulus fibrosus cells. Methods: Plate cultured annulus fibrosus cells of rabbit lumbar intervertebral disc were randomly divided into 6 groups: group A (the control group without drugs), group 13 (10μmol/L Sodium Nitroprusside, SNP), group C (100μmol/L SNP), group D (200μmol/L SNP), group E (administrating 100μmol/L SNP and 0. 05mg/ml Niacinamide), and group F (100μmol/L SNP and 0.5mg/ml Niacinamide). After 72 hours' culture, cell proliferation, intracellular ATP content, cell nitric oxide synthase activity, mitochondrial membrane potential were detected respectively. Results:After 72 hours, the intracellular cells NOS content increased and ATP content decreased with increasing concentration of SNP. There were significantly difference between control group and treatment group (P〈0. 05). Cell membrane potential decreased in SNP groups, which was reversed in Niacinamide group. Compared to SNP groups, Nicotinamide induced cell proliferation in a dose-dependent manner (P〈0.05). Conclusion: The excess NO can damage mitochondrial metabolic function of rabbit annulus fibrosus cell. Thus, inhibiting nitric oxide synthesis and protecting disc mitochondrial metabolic function might be effective to prevent disc degeneration.
出处 《中国中医骨伤科杂志》 CAS 2009年第9期6-9,共4页 Chinese Journal of Traditional Medical Traumatology & Orthopedics
基金 国家自然科学基金青年基金资助项目(NO.30700841)
关键词 纤维环细胞 线粒体 一氧化氮 烟酰胺 Annulus Fibrosus Cell Mitochondria Nitric oxide Niacinamide
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  • 1周泉,王拥军,施杞.椎间盘纤维环细胞的培养[J].脊柱外科杂志,2003,1(4):226-229. 被引量:13
  • 2RANNOU F, RICHETTE P, BENALLAOUA M, et al. Cyclic tensile stretch modulates proteoglycan production by intervertebral disc annulus fibrosus cells through production of nitrite oxide[J]. J Cell Biochem 2003,90 (1) : 148-157.
  • 3LIU G Z, ISHIHARA H, OSADA R, et al. Nitric oxide mediates the change of proteoglycan synthesis in the human lumbar intervertebral disc in response to hydrostatic pressure[J]. Spine,2001, 26(2) : 134-141.
  • 4WU X J, STHAL T, HU Y. The Production of Reactive Oxygen Species and the Mitochondrial Membrane Potential Are Modulated during Onion Oil-Induced Cell Cycle Arrest and Apoptosis in A549 Cells[J].J Nutr, 2006,136(3) :608-613.
  • 5MANEIRO E, MARTIN M A, ANDRES M C, et al. Mitoehondrial respiratory activity is altered in osteoarthritic human articular ehondrocytes[J]. Arthritis Rheum, 2003,48(3) : 700-708.
  • 6ANDRABI S A, SAYEED I, SIEMEN D, et al. Direct inhibition of the mitochondrial permeability transition pore: a possible mechanism responsible for anti-apoptotic effects of melatonin [J]. FASEB J,2004,18(7) :869-871.
  • 7MANEIRO E, LOPEZ-ARMADA M J, ANDRES M C, et al. Effect of nitric oxide on mitochondrial respiratory activity of human articular chondrocytes[J]. Ann Rheum Dis,2005,64(3) : 388-395.
  • 8JACOBSON J, DUCHEN M R, HOTHERSALL J, et al. Induction of mitochondriat oxidative stress in astrocytes by nitric oxide precedes disruption of energy metabolism[J]. J Neuroehem,2005, 95(2) :388-395.
  • 9RACHEK L I, GRISHKO V I, LEDOUX S P, et al. Role of nitric oxide-induced mtDNA damage in mitochondrial dysfunction and apoptosis[J]. Free Radie Biol Med,2006,40(5): 754-762.
  • 10PETRONILLI V, PENZO D, SCORRANO L, et al. The mitochondrial permeability transition, release of cytochrome c and cell death. Correlation with the duration of pore openings in situ [J]. J Biol Chem,2001,276(15) : 12030-12034.

二级参考文献20

  • 1熊晓芊,邵增务,杨述华.聚集蛋白聚糖与椎间盘退变的研究进展[J].中国脊柱脊髓杂志,2005,15(1):54-57. 被引量:18
  • 2朱庆三,翟饶生,许则民,杨有赓,姜鸿志,周秋丽.腰间盘髓核中胶原及蛋白多糖含量的测定[J].中华外科杂志,1994,32(8):463-465. 被引量:23
  • 3[1]Gruber HE, Hanley EN Jr. Recent advances in disc cell biology[J]. Spine, 2003, 28: 186-193
  • 4[2]Gruber HE, Hanley EN. Analysis of aging and degeneration of the human intervertebral disc: Comparison of surgical specimens with normal controls[J]. Spine, 1998, 23: 751-757
  • 5[3]Gruber HE, Hanley EN Jr. Ultrastructure of the human intervertebral disc during aging and degeneration: Comparison of surgical and control specimens[J]. Spine, 2002, 27: 798-805
  • 6[4]Park J-B, Kim, Han C-W,et al. Expression of receptor on disc cell in herniated lumbar disc tissue[J]. Spine, 2001, 26: 142-146
  • 7[5]Marouda A al. Factors involved in the nutrition of the human lumbar intervertebral disc: Cellularity and diffusion of glucose in vitro[J]. J Anat, 1975, 120: 113
  • 8[7]Alini M, Li W, Markovic P, et al. The potential and limitations of a cell-seeded collagen/hyaluronan scaffold to engineer: An intervertebral disc-like matrix[J]. Spine, 2003, 28: 446-454
  • 9[8]Shingo Maeda, Shoichi Kokubun. Changes with age in proteoglycan synthesis in cells cultured in vitro from the inner and outer rabbit annulus fibrosus responses to interleukin-1 and interleukin-1 receptor antagonist protein[J]. Spine, 2000, 25: 166
  • 10[9]Gruber HE, Hanley EN Jr. Human disc cells in monolayer vs 3D culture: Cell shape, division and matrix formation[J]. BMC Musculoskelet Disord, 2000, 1: 1-10

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