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运动对MS大鼠炎症状态和应激水平的影响及其可能机制研究 被引量:1

The Inflammation and Stress Level of MS Rats after Exercise and Its Possible Mechanism
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摘要 目的研究运动对MS大鼠炎症状态和应激水平的影响,探讨长期规律运动对MS的作用及对急性运动刺激的适应,为MS的运动康复提供理论参考。方法 50只SD雄性大鼠随机分为空白对照组(CG)和实验组(EG),EG大鼠采用高果糖膳食诱导MS模型,将部分MS大鼠随机分为安静组(RG)、安静与急性运动组(REG)、运动组(TG)和长期运动与急性运动组(TEG),每组8只,TG跑台运动14周,每周5 d,每天运动25 cm/s,35 min,急性运动一次35 cm/s,35 min,运动后标准方法检测大鼠血Glu,ELISA检测FINS、IL-6、CRP和CTC水平,高效液相荧光法测定NE浓度。结果膳食诱导大鼠MS模型成功;与CG相比,RG和TG大鼠血Glu、IL-6、CPR和NE水平均显著升高(P<0.01,P<0.001,P<0.001,P<0.001);与RG相比,TG大鼠血Glu、IL-6、CRP和NE水平均显著升高(P<0.05,P<0.01,P<0.01,P<0.001),但CTC水平显著降低(P<0.05);急性运动使RG大鼠IL-6、CPR和NE水平显著升高(P<0.001,P<0.05,P<0.01),而对TG大鼠无显著影响;TG大鼠在一次急性运动后CTC水平显著升高(P<0.05)。结论 (1)MS大鼠出现炎症-应激反馈机制失衡,从而诱导全身低度炎症和/或代谢性高血糖;(2)不恰当的运动会增强MS大鼠炎症水平和应激状态,诱导更多的糖原释放入血,进而加剧MS相关代谢、炎症和应激紊乱;(3)长期规律运动MS大鼠进行急性运动刺激后炎症反应降低,机体产生抗炎性适应。 Objective The purpose of this study is to examine the effects of exercise on inflammation and stress status in MS rats. To investigate the effects of long- term exercise on MS and the adaptation to acute exercise. So as to provide experi- mental data for sports rehabilitation of MS. Methods 50 SD rats were randomly divided into control group (CG) and experi- mental group (EG) , EG was bred with high fructose-food to build MS rat model, Take 32 MS rats randomly divided into four groups, rest group (RG), rest group with acute exercise (REG), training group (TG) and training group with acute exercise (TEG). Training consisted of treadmill running: 5 days/week for 14 weeks, at 25 cm/s for 35 min. The acute ex- ercise consisted of a single session of 35 min at 35 em/s. Glucose was determined by standard methods . Circulating concen- trations of IL -6, CRP and CTC were determined by ELISA, and that of NA was determined by HPLC. Results The MS model were induced ; Compared with CG, circulating levels of Glu, IL - 6, CPR and NE in RG and TG rats were significant- ly increased(P 〈0. 01, P 〈0. 001, P 〈0. 001, P 〈0. 001 ). Compared with RG, circulating levels of Glu,IL -6,CPR and NE in TG rats were significantly increased(P 〈0. 05, P 〈0. 01, P 〈0. 01, P 〈0. 001 ), while CTC was significantly de- creased( P 〈 0.05 ). Acute exercise increased IL - 6, CRP, and NE in RG rats(P 〈 0. 001, P 〈 0.05, P 〈 0. 01 ), but not in TG rats. CTC was increased after the acute exercise in TG rats only ( P 〈 0.05 ). Conclusions ( 1 ) Animals with MS present a dysregnlation in the feedback mechanism of inflammation and stress which can contribute to systemic low - grade inflammation and/or hyperglycaemia. (2) An inappropriate exercise intensity can enhance inflammation levels and stress state in MS rats , and induce more glycogen released into the blood, contributing to the metabolic, inflammatory, and stress disorders associated with MS. (3) The reduced inflammatory response in REG rats indicates that long - term exercise induces a positive adaptation in the response to acute exercise.
作者 姬红丽 毕丹
出处 《西安体育学院学报》 CSSCI 北大核心 2013年第5期600-605,共6页 Journal of Xi'an Physical Education University
基金 天津商业大学科研基金项目(0090-1021Y101129)
关键词 运动 代谢综合症 炎症 应激 exercise metabolic syndrome inflammation stress
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参考文献25

  • 1Eckel R H,Grundy S M, Zimmet P Z. The metabolic syn-drome [J]. The Lancet,2005 ,365(9468) : 1415-1428.
  • 2Wellen K E,Hotamisligil G S. Inflammation,stress and dia-betes [J]. J Clin Invest,2005, 115(5):1111-1119.
  • 3Teixeira de Lemos E, Reis F, Baptista S, et al. Exercisetraining decreases proinflammatory profile in Zuckerdiabetic(type 2) fatty rats[ J]. Nutrition,2009,25 (3) :330-339.
  • 4Martin -Cordero L, Garcia J J, Hinchado M D, et al. Habit-ual physical exercise improves macrophage IL-6 and TNF-aderegulated release in the obese zucker rat model of the met-abolic syndrome [ J]. Neuroimmunomodulation,2011(18):123-130.
  • 5Besedovsky H 0,Del Rey A. Physiology of psychoneuroim-munology :Apersonal view[ J]. Brain, Behavior and Immu-nity,2007, 21(1) :3444.
  • 6Elenkov I J,Iezzoni D G,Daly A, et al. Cytokine dysregu-lation,inflammation and well-being[ J]. Neuroimmunomod-ulation,2005(12) :255-269.
  • 7Meltzer J C, MacNeil B J, Sanders V,et al. Stress -inducedsuppression of in vivo splenic cytokine production in the ratby neural and hormonal mechanisms[ J]. Brain, Behavior,and Immunity,2004, 18(3) :262-273.
  • 8Hotamisligil G S. Inflammation and metabolic disorders[J]. Nature,2006,444:860-867.
  • 9陈巍,李娟,陈庆合.运动促进骨骼肌功能康复改善代谢综合征的研究进展[J].中国康复医学杂志,2012,27(6):577-582. 被引量:11
  • 10Ortega E. Neuroendocrine mediators in the modulation ofphagocytosis by exercise:physiological implications[ J]. Ex-ercise Immunology Review, 2003 (9 ) :70-93.

二级参考文献46

  • 1Li L J. Exercise and hormesis: activation of cellular antioxidant signaling pathway[J]. Ann NY Acad Sci, 2006, 1067: 425-435.
  • 2Zsolt Rad. Age-associated increases in oxidative stress and nuclear transcription factor-r.B activation are attenuated in rat liver by regular exercise[J].The Faseb Journal, 2004, 1096: 471-474.
  • 3Susan V B. Repeated bouts of aerobic exercise lead to reductions in skeletal muscle free radical generation and nuclear factor kappaB activation[J]. Physiol, 2008, 596(16): 3979-3990.
  • 4William J, Li Y E Fatiguing exercise reduces DNA binding activity of NF-kappaB in skeletal muscle nuclei[J]. Appl Physiol, 2004, 97(5): 1740-1745.
  • 5Toldy A. The effect of exercise and nettle supple- mentation on oxidative stress markers in the rat brain[J]. BrainRes Bull, 2005, 65(6): 487-493.
  • 6Li L J. Modulation of skeletal muscle antioxidant de- fense by exercise: Role ofredox signaling[J]. Free Radic BiolMed, 2008, 44(2): 142-152.
  • 7Seo D. 12 weeks of combined exercise is better than aerobic exercise for increasing growth hormone in mid- dle-agedwomen[J].2010, 20(1): 21-26.
  • 8Si-Young Kim. Effects of exercise on cyclooxy- genase-2 expression and nuclear factor-kB DNA binding in human peripheral blood mononuclear cells natural compounds and their role in apoptotic cell signaling pathways[J]. Ann N Y Acad Sci, 2009, 1171 : 464-471.
  • 9Delhalle S, Blasius R, Dicato M, et al. Abeginner's guide to NF-kappaB signaling pathways[J]. Ann N Y AcadSci, 2004, 1030: 1-13.
  • 10Zhang L. Pathways for nuclear factor kappaB activation by angiotensin II in vascular smooth muscle: phosphorylation of p65 by Ikappa B kinase and ribo- somal kinase[J]. Circ Res, 2005, 1197(10): 975-982.

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