力竭游泳运动后大鼠伏核NF-κB、cAMP表达的变化
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摘要
目的:观察力竭游泳运动后大鼠伏核NF-κB和cAMP的表达变化,探讨力竭运动后大脑伏核的调节机制,从而为指导运动训练、临床疾病的预防和运动康复治疗提供理论依据。
     方法:选取80只SD大鼠,于适应性训练后随机分为安静对照组(n=10)和力竭组(n=70)。力竭组进行一周力竭性游泳训练后,按0h,4h,8h,12h,16h,20h,24h时间点,分别按冰水浴分离新鲜脑组织或多聚甲醛固定取脑的程序进行,前者经Western Blot和ELISA反应,分别检测伏核内NF-κB和环磷酸腺苷(cAMP)的含量变化,后者经免疫组织化学染色,观察NF-κB在伏核内的表达变化。对照组同时进行。
     结果:(1)Western Blot显示,对照组大鼠伏核内NF-κB表达较少,力竭运动后NF-κB表达明显增多。力竭运动后,8h时达到较高水平,以后维持在较高水平,于16h时达到高峰,然后才开始回落。(2)力竭运动后,0 h时阳性神经元数目与对照组无统计学意义,4h后NF-κB阳性神经元数目均显著高于对照组, 8h达到较高水平,并维持在较高水平,持续至16h达到峰值后才开始下降。(3)对照组cAMP表达较低,力竭运动后在0h时,有一过性的升高,然后有所下降,但于8h又达到高峰,以后一直维持在较高水平,至16h后才开始缓慢下降。(4)力竭运动后, NF-κB和cAMP具有明显相同的时效性关系。
     结论:(1)一周力竭游泳训练可以使大鼠大脑伏核中NF-κB与cAMP得到有效的活化。(2)一周力竭性游泳训练大鼠大脑伏核中NF-κB与cAMP两者变化趋势基本一致,提示它们可能具有协同效应。(3)NF-κB和cAMP信号通路可能作为一些与伏核相关的疾病的治疗手段,以及为指导运动训练提供理论依据。
Objective: To observe the expression of NF-κB and cAMP in Rat NAc of adult rats after exhausted swimming, and investigate the mechanism of NAc after exhausted swimming. Providing theoretical evidences for exercise training,and offering new ideas for exercise induced disease prevention and sport treatment.
     Methods: Eighty SD rats were divided into the control group (n=10) and exhausted group (n=70) after adaptive training. The fresh cerebral tissues were divided on ice water bath while the paraform-perfused brains were obtained at 0h,4h,8h,12h,16h,20h,24h after exhausted swimming for a week. The former cerebral tissues were detected by Western Blot and ELISA in order to investigate the changes of NF-κB and cAMP in NAc, however, the later perfused brains be done with frozen section, immunohistochemical staining, then the change of expression of NF-κB were observed. The same to control group.
     Results: (1). Western Blot showed, the expression of NF-κB was extremely lower in control group, but increased higher after exercise. In NAc, the expression of NF-κB increased to the higher level at 8h after exhausted swimming,then,retainned high level for a monment, peaked at 16h, then descended gradually. (2). Compared with control group, the number of NF-κB+ neurons had no significant difference at 0h. Several NF-κB+ neurons of control group distributed in the NAc dispersively while the exhausted groups expressed significantly higher after 4h, and increased to the higher level at 8h, then, retained the high level, peaked at 16h, then descended dramatically.(3). The expression of cAMP was extremely lower in control group, but transiently increased at 0h after exhausted exercise, then increased to the top at 8h ,retained high level to 16h,and descended gradually.(4). NF-κB is the same as cAMP in time course.
     Conclusion: (1). NF-κB and cAMP can be activated effectively in NAc after exhausted exercise. (2).the tendencys of change of NF-κB and cAMP in NAc after exhausted exercise are similar, It is suggested that they have synergistic effect. (3). NF-κB and cAMP signals passways may be offering new therapy means for relative-NAc-disease,and providing theoretical evidences for exercise training.
引文
[1] Sen R, Baltimore D. Multiple nuclear factors interact with the immunoglobulin enhancer sequences. Cell ,1986 , 46 : 705-716.
    [2] Chen F, Castranova V, Shi X. New insights into the role of nuclear factor-κB in cell growth regulation. Am J Pathol, 2001,159: 387-397.
    [3] Ghosh S, May M J, Kopp E B. NF-κB and Rel proteins: Evolutionarily conserved mediarors of immune responses. Annu Rev Immunol ,1998 ,16: 225-260.
    [4] Baldwin A. The NF-κB and IκB proteins: New discoveries and insights.Annu Rev Immunol ,1996 ,14: 649-681.
    [5]郭双平,王文亮,翟宇强.核因子NF-κB的研究进展.中国病理学杂志, 2000, 29(5): 379-380.
    [6] John J Haddad. Redox and oxygen-sensitive transcription factors in the regulation of oxidant-mediated lung injury: role for nuclear factor-κB , Critical Care 2002 , 6: 481-490.
    [7] C. Leeuwenburgh,J. W. Heinecke Oxidative Stress and Antioxidants in Exercise . Current Medicinal Chemistry , 2001, 8, 829-838.
    [8] Hang CH , Shi JX , Li JS ,et al . Concomitant upregulation of nuclear factor-κB activity, proinflammatory cytokines and ICAM-1 in the injured brain after cortical contusion trauna in a rat model. Neurol India, 2005, 53(3): 312-317.
    [9]路阿明,路爱云.耐力训练与中枢神经系统细胞凋亡的实验研究.体育与科学. 2003; 24(5): 69-71.
    [10]朱全,浦钧宗.大鼠游泳训练在运动实验中的应用.中国运动医学杂志, 1996, 15(2): 125.
    [11] Edwards RHT, et al. Biochemical bases of fatigue in exercise performance catastro- phe theory of muscular fatigue in knuttgln HG. Biochemistry of exercise human kinetics. Publishers , Inc, 1983; 3-2.
    [12] Baeuerle PA, Henkel T . Function and activation of NF-kappaB in the immune system Annu Rev Immunol 1994;12: 41-79.
    [13] Jarosinski KW, Whitney LW, Massa PT. Specific deficiency in nuclear factor kappaB activatinn in neurons of the central nervous system.Lab Invest 2001; 81(9):1275-88.
    [14] Li X.Stark GR. NF-kappaB-dependent signaling pathways. Exp Hematol. 2002 , 30(4): 285-296.
    [15] Iwai K ,Lee BR ,Hashiguchi M , et al. IkB-alpha-specific transcript regulation by theC- terminal end of c-Rel . FEBS Lett, 2005, 579(1):141-144.
    [16] Liou HC . Regulation of the immune system by NF-kappaB and IkappaB . J Biochen Mol Biol, 2002, 35(6): 537-546.
    [17] Li X Massa PE , Hanidu A ,et al. IKKalpha , IKKbete ,and NEMO/IKKgamma are each required for the NF-kappaB-mediated inflammatory response program . J Biol Chem , 2002, 277(47): 45129-45140.
    [18] Kaltschmidt C , Kaltschmidt B , Neumann H , et al . Mol Cell Bi-ol , 1994, 14 : 3981 - 3992.
    [19] O’Neill LAJ , Kaltschmidt C. Trends Neurosci , 1997 , 20 :252 -258.
    [20] Grilli M, Goffi F , Memo M, et al . J Biol Chem, 1996 , 271 :15002 - 15007.
    [21] Kaltschmidt B , Uherek M, Volk B , et al . Proc Natl Acad Sci USA , 1997 , 94 : 2642 - 2647.
    [22]陈立朝,许民辉,周继红. CRH通过PKA途径调节大鼠下丘脑CRH表达的研究.第三军医大学学报, 2004, 26(16): 1459-1462.
    [23] Grammatopoulos D K, Randeva H S , Levine M A , et al . Urocortin , but not corticotrophin -releasing hormone ( CRH) , activates the mitogen-activated protein kinase signal transduction pathway in human pregnant myometrium: an effect mediated via R1alpha and R2 beta CRH receptor subtypes and stimulation of Gq-proteins [J ] . Mol Endocrinol , 2000 , 14 (12) : 2076 - 2091.
    [24]郭世炳、句海松.运动与氧自由基损伤[J].中国运动医学杂志, 1990, 9(3): 161.
    [25]倪耀华,王秀业.不同运动强度对血浆氧自由基代谢水平的研究[J].四川体育科学, 2000,1:15-16.
    [26] Davies, KJ, Quintanilha, ATBrooks. GA, eta1. Free radicals and tissue damage produced by exercise[J]. Biochem.Biophys.Res. Commun.1982, 107:l198-1205.
    [27]陈英杰,郭庆芳,赵保路.等. ESR研究大鼠疲劳时不同类型肌纤维的自由基变化[J].中国运动医学杂志, 1991, 10(3): 135-139.
    [28]丁树则,许豪文,程伯基.运动内源性自由基对大鼠心肌线粒体膜的影响[J].生物化学与生物物理学报, 1991, 23(4): 305-309.
    [29]张勇,时庆德,文立,等.运动性疲劳的线粒体膜分子机制研究.I.急性力竭运动中线粒体电子漏引起质子漏增加及其相互作用[J].中国运动医学杂志. 1999, l8(3): 236-239.
    [30]衣雪洁,常波,王和平.力竭运动对大鼠胃组织脂质过氧化水平的影响.沈阳体育学院学报,1997,(4):4O-42.
    [31]赖红梅.力竭运动恢复期大鼠血液中自由基的研究.体育与科学, 1998, 19(1): 59-61.
    [32]张均,邓蜀李,刘扬,等.运动对大鼠心肌线粒体功能的影响.北京体育大学学报, 2003, 26(2): 198-200.
    [33]李晖,辛东,李静先,等.递增负荷力竭性运动时大鼠血液氧化,抗氧化能力及RBCM生物物理特性的研究.中国运动医学杂志, 2001, 20(3): 256-259.
    [34]陈筱春,文质君.急性力竭运动对小鼠器官脂质过氧化反应的比较. 2001, (22): 23-14..
    [35] Nakai M, Qin ZH, Wang Y, et al. Brain Res Mol Brain Res, 1999, 64 : 59-68.
    [36]王海蓉,李建军,蒋锡嘉,许家,王利.核因子-κB与氧化应激.心血管病学进展. 2002, (23), 166-170.
    [37] O gata N, Yamamato H, Kugiyama K, et al. Involvement of protein kinase C in superoxide anion-induced activation of nuclear factor-κB in human endo thelial cells[J]. Cardio l Res, 2000, 513-521.
    [38] Mason NJ, Artis D, Hunter CA. New lessons from old pathogens:what parasitic infections have taught us about the role of nuclear factor-kappaB in the regulation of immunity [J]. Immunol Rev, 2004, 201: 48-56.
    [39] Vasudevan KM, Gurumurthy S , Rangnekar VM. Suppression of PTEN expression by NF-kappa B prevents apoptosis. Mol Cell Biol, 2004, 24(3): 1007-1021.
    [40] Kim EJ Kwon KJ , Park JY, et al. Effects of peroxisome proliferator-activated receptor against on LPS-induced neuronal death in mixed cortical neurons: associated with Inos and COX-2[J]. Brain Res, 2002, 941(1-2): 1-10.
    [41] Kaur P, Kaur G, Bansal MP. Tertiary-buty1 hydroperoxide induced oxidative stress and male reproductive activity in mice: role of transcription factor NF-kappaB and testicular antioxidant enzymes. Reprod Toxicol. 2006, 22(3): 479-84.
    [42] Chiao PJ, Miyamoto S, Verma IM. Autoregulatoin of IkB-αactivity. Proc Natl Acad Sci USA, 1994, 91: 28-32.
    [43] SaekiK, YuoA. Distinct involvement of cAMP response element dependent trans- criptions in functional and morphological maturation during retinoid mediated human myeloid differentiation[J]. Journal of Leukocyte Biology, 2003, 73 (5) : 673-681.
    [44] Garg A, Aggarwal BB. Nuclear transcription factor-kappaB as a target for cancer drug development[J]. Leukemia, 2002 , 16 (6) :1053-1068 .
    [45] JaramilloM, OlivierM. Hydrogen peroxide induces murine macrophage chemokine gene transcription via extra cellular signal regulated kinase and cyclicadenosine 5′- monopho- sphate (cAMP) dependent pathways: involvement of NF-kappaB activator protein and cAMP response element binding protein[J]. J Immunol, 2002, 169 (12) : 7026-7038.
    [46] Liu S Z, Su X, Zhang Y C et al . Signal transduction in lymphocytes after low dose radiation . Int J Occup Med Toxicol ,1994 , 3 (2) : 107-117.
    [47] Sen R, Baltimore D A. Inducibility of kappa immunoglobulin enhancer-binding protain NF-κB by a post-translational mechanism. Cell , 1986 , 47 : 921-928.
    [48]于秉治.蛋白激酸C研究的最新进展.生物化学与生物物理进展, 1994 , 21 (4) : 308-312.
    [49] Femandez-Espejo E. How does the nucleus accumbens function. Rev Neurol, 2000, 30(9): 845-849.
    [50] Hunot S, Brugg B, Ricard D, et al. Proc Natl Acad Sci USA, 1997, 94: 7531- 7536.
    [51] Kaltschmidt B, Uherek M, Volk B, et al. Proc Natl Acad Sci USA, 1997, 94: 2642 -2647.
    [52]郑瑞茂,宋韫韬,祝世功.钙离子调节的转录因子NF-κB激活参与小鼠记忆功能与行为调控. Nature Neuroscience, 2003, 6: 1072-1078.
    [53]王丽,章军建,刘涛. PKA-CREB信号转导通路在大鼠慢性脑缺血所致认知功能障碍中的作用. Chin J Clin Neurosci 2006, 14 (5) :449-453.
    [54] Abel T, Nguyen PV, Barad M, et al. Genetic demonstration of a role for PKA in the late phase of LTP and in hippocampus-based long- term memory[J]. Cell, 1997 , 88: 615-626.
    [55] Toru M. Biological rsearch on schizophrenia. Psychiatry. Clin Neurosic, 1998, 52 : 170-172.
    [56] Alderson HL, Parkinson JA, Robbins TW, et al. The effects of excitotoxic lesions of the nucleus accumbens core or shell regions on intravenous heroin self-administration . Psychopharmacology (berl), 2001, 153(4): 455-463.
    [1]方允中.营养与活性氧[J] .生理科学, 1989 , 9(4) : 5 - 9.
    [2] Kanter MM, et al . Serum lipid levels and lipid peroxidition in ultramarathon runners[J] . Annals of Sports Medicine , 1986 , 3 : 9.
    [3]叶新钢,刘家玉.运动性血红蛋白尿血症红细胞脂质过氧化的测定[J] .体育学刊,1996 , (3) :50.
    [4]刘丽萍,柴戬臣,容仕霖,等.游泳训练对大鼠心、肝、肾组织和血清中自由基代谢、CK和LDH活性的影响[ J ] .体育科学,1999 ,19 (1) :80-81.
    [5]刘丽萍,柴戬臣,唐卫平,等.游泳训练对大鼠肝组织自由基代谢及肝脏超微结构的影响[ J ] .中国运动医学杂志, 1998 , 17.
    [6]郭世炳,句海松.运动与氧自由基损伤[J] .中国运动医学杂志, 1990 , 9(3) :161.
    [7]倪耀华,王秀业.不同运动强度对血浆氧自由基代谢水平的研究[J].四川体育科学, 2000 ,1 : 15-16.
    [8]胡红梅.运动性内源自由基对大鼠心肌线粒体功能的影响[J].运动医学杂志, 1998 ,17 (1) : 24-25.
    [9]时庆德.运动性疲劳的线粒体膜分子研究在运动性氧的自由基代谢途径再探讨[ J ] .运动医学杂志, 2000 , 19 (1) : 43 - 44.
    [10]许家佗,张志枫,孙鸿杰.力竭性运动前后的脉图观察研究[J].中国运动医学杂志, 2002, 21 (1) : 44 - 47.
    [11]张勇.运动性疲劳状态下线粒体膜生物学特征的研究I:力竭运动后大鼠心肌和骨骼肌线粒体膜脂质过氧化变化[J].体育科学, 1994, 14 (4) : 67 - 70.
    [12]张钧.力竭运动对大鼠心肌线粒体游离钙及磷脂酶A2的影响[J].中国运动医学杂志, 1998, 17 (1) : 26 - 27.
    [13]毛丽娟,李传珠.运动对大鼠心肌GSH、GSSG含量及GSH /GSSG的影响[J].成都体育学院学报, 2004, 30 (1) : 75 -78.
    [14]乔玉成.谷氨酰胺对力竭性运动大鼠腓肠肌抗氧化能力效果研究[J].成都体育学院学报, 2002, 2 (2) : 87 - 88.
    [15]金其贯.慢性力竭性训练对大鼠骨骼肌细胞凋亡的影响[J].体育与科学, 1999, 20: 23 - 28.
    [16]王瑞元,苑玉和,冯炜权.一次力竭性离心运动后大鼠骨骼肌α-action基因表达及针刺对其影响.北京体育大学学报, 2002, 25 (2) : 189 - 221
    [17]李发琪.大鼠运动力竭后肠系膜毛细血管血流动力学变化的研究[J].中国运动医学杂志, 1999, 18 (1) : 34 - 35.
    [18]赵敬国.力竭运动后大鼠胃组织一氧化氮含量的变化[J].中国运动医学杂志, 2003, 22 (2) : 198 - 190.
    [19]金其贯.高压氧对急性力竭性运动后血乳酸清除和肝酶谱恢复的影响[J].体育与科学, 1997, 18 (1) : 34 - 39.
    [20]郭林.力竭运动导致大鼠急性肾小管损伤机制的研究[J].中国运动医学杂志, 1999, 18 (2) : 129 - 133.
    [21]李辉.递增负荷运动至力竭大鼠肾脏自由基产生及氧化抗氧化能力的研究[J].中国运动医学杂志, 1999, 18 (1) : 31- 33.
    [22]衣雪杰.力竭游泳对红细胞膜的影响[J].中国运动医学杂志, 2001, 20 (2) : 139 - 141.
    [23]尤春英,岑浩望,田亚平,等.不同负荷跑台训练对大鼠脑自由基代谢及其防御系统酶活性的影响[J].中国运动医学杂志, 2001, 20 (2) : 202 - 204.
    [24] MEEUSEN RK. Endurance Training Effects on Neurotransmitter Release in Rat Striatum: an in Vivo Microdialysis Study[J]. Acta Physiol Scand, 1997, 159 (4) : 335 - 341.
    [25]王斌,张蕴琨,李靖,等.力竭运动对大鼠纹状体、中脑及下丘脑单胺类神经递质的影响[J].中国运动医学杂志, 2002, 21 (2) : 248 - 252.
    [26] Baeuerle PA. IκB-NF-κB structures: at the interface of inflammation control . Cell , 1998 , 95 : 729-731.
    [27] Nanxin Li,Michael K. Is NF-κB the sensor of oxidative stress[J]? FASEB J , 1999, 13: 1137-1143.
    [28] Pieper GM ,Okls C, Hilton G, et al. A ntioxidant treatment inhibits activation of myocardial nuclear factor kappa B and inhibits nitrosylation of myocardialheme protein in cardiac transplant rejection [J]. A ntioxid Redox Signal, 2001, 3: 81-88.
    [29] Kathy K, Griendling , Dan S , et al. Modulation of protein kinase activity and gene expression by reactive oxygen species and their role in vascular physiology and pathophysiology [J] . Arterioscler Thromb Vasc Biol , 2000 , 20 : 2175 - 2183.
    [30]金其贯,邓荣华,李宁川.过度训练对大鼠心肌细胞凋亡的影响[J] .中国运动医学杂志, 2000 , 19(40) : 356.
    [31] Liu SL ,Shi DY,Shen ZH ,et al . Effects of glutamine on tumor growth and apoptosis of hepatoma cells[J] . Acta Pharmacol Sin , 2000 , 21 (7) : 668.
    [32]陈立朝,许民辉,周继红. CRH通过PKA途径调节大鼠下丘脑CRH表达的研究.第三军医大学学报, 2004, 26(16): 1459-1462.
    [33] Grammatopoulos D K, Randeva H S , Levine M A , et al . Urocortin , but notcorticotrophin-releasing hormone (CRH) , activates the mitogen-activated protein kinase signal transduction pathway in human pregnant myometrium: an effect mediated via R1alpha and R2 beta CRH receptor subtypes and stimulation of Gq-proteins [J] . Mol Endocrinol , 2000 , 14 (12) : 2076 - 2091.
    [34] Natarajan V. Oxidants and signal transduction in vascular endothelium[J] . Lab Clin Med ,2004 ,125 : 26-37.
    [35] SaekiK, YuoA. Distinct involvement of cAMP-responseelement–dependent transcriptions infunctional and morphological maturation during retinoid–mediated human myeloid differentiation[J]. Journal of Leukocyte Biology, 2003 , 73 (5) : 673-681 .
    [36] JaramilloM, OlivierM.Hydrogen peroxide induces murine macrophage chemokine gene transcription via extra cellular signal-regulated kinase and cyclic adenosine 5′- monophosphate (cAMP)-dependent pathways: involvement of NF-kappaB, activator protein1 , and cAMP responseelement binding protein[J]. JImmunol, 2002 , 169 (12) : 7026-7038 .
    [37] GargA, AggarwalBB. Nuclear transcription factor-kappaB as a target for cancer drug development[J]. Leukemia, 2002 , 16 ( 6 ) : 1053-1068.

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