不同强度运动对糖尿病动脉硬化及血浆NF-κB、IL-6、IL-10、TNF-α水平的影响
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摘要
目的：通过建立SD大鼠糖尿病动脉粥样硬化模型,检测不同强度运动干预后大鼠主动脉血管病变情况及血浆中NF-κB、IL-6、IL-10、TNF-α等炎症相关因子的变化,探讨运动对糖尿病动脉粥样硬化主动脉病变组织的影响以及运动与炎症相关因子NF-κB、L-6、IL-10、TNF-α的关系,为糖尿病并发症的运动治疗提供理论依据。方法：(1)将100只SD大鼠随机分为对照组(20只)及糖尿病动脉粥样硬化组(80只),其中糖尿病动脉粥样硬化组又分为4个亚组：模型组、少量运动组、中等量运动组、大量运动组,每个亚组各20只大鼠。对照组给予普通膳食,余四组给予高脂高糖膳食(常规饲料加10%炼猪油、10%蔗糖、5%蛋黄),饲养4周后,对照组SD大鼠腹腔注射0.1mol/l柠檬酸缓冲液,余4组SD大鼠腹腔注射STZ (30mg/kg),继续原方案饲养6周,建立糖尿病动脉粥样硬化大鼠模型。(2)观察计算糖尿病动脉粥样硬化模型大鼠的力竭游泳时间,然后以100%、70%及40%的力竭时间分别为大量运动、中等量运动和小量运动的干预时间,本实验中具体时间为：30min、21min、12min。1次/天,6天/周,共运动干预6周。断头处死,采集血标本及主动脉组织标本。采用ELISA法测定各组大鼠血浆中NF-κB、IL-6、IL-10、TNF-α水平。主动脉组织福尔马林固定、石腊包埋、切片后,HE染色,显微镜下分析主动脉病理变化及病变程度。结果：(1)各组大鼠主动脉HE染色结果显示：对照组大鼠主动脉未见异常：模型组大鼠主动脉多呈动脉硬化(AS)Ⅳ期改变；小量运动组及大量运动组主动脉组织多呈AS Ⅱ期改变；中等量运动组主动脉组织多呈ASⅠ期改变。(2)与对照组相比,无论运动前或运动后,各组大鼠血浆NF-κB、IL-6、IL-10及TNF-α等因子的水平均增高(P<0.001)；与模型组相比,运动后各不同强度运动组NF-κB、IL-6、IL-10水平均降低(P<0.001)；与小量运动组相比,运动后中等量运动组NF-κB、IL-10水平降低(P<0.05),大量运动组未表现出统计学差异,中等量运动组和大量运动组IL-6均降低(P<0.001)；与中等量运动组相比,运动后大量运动组IL-10浓度较高(P<0.001)；运动后,模型组和三个运动组间TNF-α水平无差异性(P>0.05),三个运动组间相比较,也无统计学意义(P>0.05)。各组运动前后自身相比较,除对照组外,余四组运动后NF-κB、 IL-6、IL-10水平均下降(P<0.001),各组TNF-α水平在运动前后未表现出差异性(P>0.05)。(3)糖尿病动脉粥样硬化大鼠主动脉组织AS病变程度与炎症相关因子NF-κB、IL-6、IL-10及TNF-α呈正相关,相关系数分别为(r=0.773,P<0.05)、(r=0.765,P<0.05)、(r=0.797,P<0.05)、(r=0.532,P<0.05)。结论：运动对糖尿病动脉粥样硬化的形成具有延缓、抑制作用,尤以中等强度运动作用最为明显。糖尿病动脉粥样硬化大鼠血浆NF-κB、IL-6、IL-10、TNF-α等因子的水平明显增高。运动可降低糖尿病动脉粥样硬化大鼠中炎症相关因子NF-κB、IL-6、IL-10及TNF-α的水平,但并不与运动强度成正比,中等强度的运动对NF-κB、IL-6、IL-10的影响较为明显,三种强度运动对TNF-a的影响无差异性。糖尿病动脉粥样硬化动脉组织病变程度与血浆NF-κB、IL-6、IL-10、TNF-α等因子水平呈正相关。
Objective:to evaluate the change of the level of factors NF-KB、IL-6、IL-10and TNF-a in serum of diabetes atherosclerosis rat and the change of arterial vessel wall after different intensity exercise by establishing the model of diabetes atherosclerosis with Sprague-Dawley rats. Indentify the relation between exercise and the arterial vessel wall of diabetes atherosclerosis rat, exercise and inflammation factors NF-KB、IL-6、IL-10and TNF-a, provide the theory of the treatment of diabetes complications by exercise.Methods:(1)100rats were divided into control group(20rats) and diabetes atherosclerosis group(80rats) randomly, the diabetes atherosclerosis group were divided into four subgroups:model group, low intensity exercise group, moderate intensity exercise group, high intensity exercise group,20rats every group. The control group was given normal diet, four subgroups were given high-fat-high-sugar diet (add10%fat and10%sugar and5%egg to normal diet). 4weeks later, the control group was injected with vehicle of0.1mol/1citric acid buffer via abdominal, four subgroups were injected low-dosage of30mg/kg streptozotocin (STZ) to establish rat model of diabetes mellitus. Then continued their diets as before for6weeks until the model of diabetes atherosclerosis were established.(2) Observed the exhaustion time of diabetes atherosclerosis animals in swimming exercise, then the exhaustion time was determined as the time of high intensity exercise,70%and40%of the exhaustion time were determined as the time of moderate intensity exercise and low intensity exercise respectively, the exact time in this study were30min,21min,12min. There different exercise intensity groups swam6d/w, for6weeks. Then all animals were killed by decapitation with anesthesia, the blood and aorta were immediately collected.The levels of factors NF-KB、IL-6、IL-10and TNF-a were measured by ELISA. The arterial vessel wall tissues were fixed with formalin, made paraffin blocks, and seetions of arterial vessel wall were stained with hematoxylin and eosin(HE), then analyzed their pathological changes through the microscope.Results:(1) the rat aorta are serially sectioned, the aortas of control group don't have any abnormality. aortas of diabetes atherosclerosis group are mainly in the IV phase of atherosclerosis, aortas of low intensity exercise group and high intensity exercise group are mainly in the Ⅱ phase of atherosclerosis, aortas of moderate intensity exercise group are mainly in the I phase of atherosclerosis. (2) Compared to control group, the levels of NF-KB, IL-6, IL-10and TNF-a of four subgroups are all higher than control group either before exercise or after exercise(P<0.001); compared to model group, the levels of NF-KB, IL-6, IL-10of three exercise groups are reduced after exercise (P<0.001); compared to low intensity exercise group, the levels of NF-KB and IL-10of moderate intensity exercise group are lower after exercise (P<0.05), the level of IL-6of moderate intensity exercise group and high intensity exercise group are lower after exercise too(P<0.001); compared to moderate intensity exercise group, the level of IL-10of high intensity exercise group is higher(P<0.001)after exercise; the levels of TNF-a of three exercise groups have no difference with model group after exercise (P>0.05), and there is no difference among three exercise groups either(P>0.05). When every group compared to themselves before exercise, except the control group, the levels of NF-KB, IL-6, IL-10of four subgroups decreased obviously(P<0.001), but not TNF-a.(3) The degree of pathological changes of the aorta tissue of diabetes atherosclerosis rat was positively correlated with the serum levels of NF-KB, IL-6, IL-10and TNF-a, the correlation coefficients were (r=0.773, P<0.05)、(r=0.765, P<0.05)、(r=0.797, P<0.05)、(r=0.532, P<0.05) respectively.Conclusions:exercise plays an important role in the prevention, delay of the formation of diabetes atherosclerosis, especially the moderate intensity exercise. The levels of factors NF-KB, IL-6, IL-10, TNF-α markedly increase in diabetes atherosclerosis. Exercise can reduce the levels of factors NF-KB, IL-6, IL-10, TNF-α of diabetes atherosclerosis rat, but the effect isn't directly proportional to the intensity of exercise, the moderate intensity exercise have higher effect of factors NF-KB, IL-6, IL-10compared to the other two intensity exercise, the three different intensity exercise have no effect on TNF-α. The degree of pathological changes of diabetes atherosclerosis was positively correlated with the serum levels of NF-KB, IL-6, IL-10and TNF-α.
Objective:to evaluate the change of the level of factors NF-KB、IL-6、IL-10and TNF-a in serum of diabetes atherosclerosis rat and the change of arterial vessel wall after different intensity exercise by establishing the model of diabetes atherosclerosis with Sprague-Dawley rats. Indentify the relation between exercise and the arterial vessel wall of diabetes atherosclerosis rat, exercise and inflammation factors NF-KB、IL-6、IL-10and TNF-a, provide the theory of the treatment of diabetes complications by exercise.Methods:(1)100rats were divided into control group(20rats) and diabetes atherosclerosis group(80rats) randomly, the diabetes atherosclerosis group were divided into four subgroups:model group, low intensity exercise group, moderate intensity exercise group, high intensity exercise group,20rats every group. The control group was given normal diet, four subgroups were given high-fat-high-sugar diet (add10%fat and10%sugar and5%egg to normal diet). 4weeks later, the control group was injected with vehicle of0.1mol/1citric acid buffer via abdominal, four subgroups were injected low-dosage of30mg/kg streptozotocin (STZ) to establish rat model of diabetes mellitus. Then continued their diets as before for6weeks until the model of diabetes atherosclerosis were established.(2) Observed the exhaustion time of diabetes atherosclerosis animals in swimming exercise, then the exhaustion time was determined as the time of high intensity exercise,70%and40%of the exhaustion time were determined as the time of moderate intensity exercise and low intensity exercise respectively, the exact time in this study were30min,21min,12min. There different exercise intensity groups swam6d/w, for6weeks. Then all animals were killed by decapitation with anesthesia, the blood and aorta were immediately collected.The levels of factors NF-KB、IL-6、IL-10and TNF-a were measured by ELISA. The arterial vessel wall tissues were fixed with formalin, made paraffin blocks, and seetions of arterial vessel wall were stained with hematoxylin and eosin(HE), then analyzed their pathological changes through the microscope.Results:(1) the rat aorta are serially sectioned, the aortas of control group don't have any abnormality. aortas of diabetes atherosclerosis group are mainly in the IV phase of atherosclerosis, aortas of low intensity exercise group and high intensity exercise group are mainly in the Ⅱ phase of atherosclerosis, aortas of moderate intensity exercise group are mainly in the I phase of atherosclerosis. (2) Compared to control group, the levels of NF-KB, IL-6, IL-10and TNF-a of four subgroups are all higher than control group either before exercise or after exercise(P<0.001); compared to model group, the levels of NF-KB, IL-6, IL-10of three exercise groups are reduced after exercise (P<0.001); compared to low intensity exercise group, the levels of NF-KB and IL-10of moderate intensity exercise group are lower after exercise (P<0.05), the level of IL-6of moderate intensity exercise group and high intensity exercise group are lower after exercise too(P<0.001); compared to moderate intensity exercise group, the level of IL-10of high intensity exercise group is higher(P<0.001)after exercise; the levels of TNF-a of three exercise groups have no difference with model group after exercise (P>0.05), and there is no difference among three exercise groups either(P>0.05). When every group compared to themselves before exercise, except the control group, the levels of NF-KB, IL-6, IL-10of four subgroups decreased obviously(P<0.001), but not TNF-a.(3) The degree of pathological changes of the aorta tissue of diabetes atherosclerosis rat was positively correlated with the serum levels of NF-KB, IL-6, IL-10and TNF-a, the correlation coefficients were (r=0.773, P<0.05)、(r=0.765, P<0.05)、(r=0.797, P<0.05)、(r=0.532, P<0.05) respectively.Conclusions:exercise plays an important role in the prevention, delay of the formation of diabetes atherosclerosis, especially the moderate intensity exercise. The levels of factors NF-KB, IL-6, IL-10, TNF-α markedly increase in diabetes atherosclerosis. Exercise can reduce the levels of factors NF-KB, IL-6, IL-10, TNF-α of diabetes atherosclerosis rat, but the effect isn't directly proportional to the intensity of exercise, the moderate intensity exercise have higher effect of factors NF-KB, IL-6, IL-10compared to the other two intensity exercise, the three different intensity exercise have no effect on TNF-α. The degree of pathological changes of diabetes atherosclerosis was positively correlated with the serum levels of NF-KB, IL-6, IL-10and TNF-α.
引文
[1] Zimmet P, Alberti KG, Shaw J. Global and societal implications of the diabetes epidemic[J]. Nature,2001,414 (6865):782.
[2] Ross R. Atherosclerosis-An inflammatory disease[J]. New Engl J Med.1999,340(2):115-216.
[3] 范乐明.动脉粥样硬化炎症机制的再认识[J].中国动脉粥样硬化杂志,2005,13(3)：249-253.
[4] Catheart MK. Regulation of superoxide anion production by NADPH oxidase in monocytes/macrophages coniributions to atherosclerosis[J]. Arterioseler Thramb Vase Biol,2004,24 (1):23-28.
[5] Maiti R, Agrawal N. Atherosclerosis in diabetes mellitus: Role of inflammation [J]. Indian J Med Sci.2007,61(5):292-305.
[6] Sunsaneevithayakul P, Boriboohirunsarn D, Sutanthavibul A, etc.Risk factor-based selective screening program for gestational diabetes mellitus in Siriraj Hospital:result from clinical practice guideline[J]. J Med Assoc Thai,2003,86(8) 708-714.
[7] 吴伟华,张巾超,于江波,等.2型糖尿病及合并大血管病变糖尿病患者C反应蛋白水平观察[J].中华内分泌代谢杂志,2003,19(4)：257-259.
[8] Barzilay JI, Abraham L, Heckbert SR, etc.The relation of markers of inflammation to the development of glucose disorders in the elderly:the Cardiovascular Health Study [J]. Diabetes,
2001,50(10)：2384-2389.
[9] 郭立新.血脂异常与动脉粥样硬化的研究进展[J].世界医学杂志,2002,11(6)：42-44.
[10] 杨永宗.动脉粥样硬化性心血管病基础与临床[M].北京：科学出版社,2004.
[11] Rauramaa R, Halonen P, Vaisanen SB, etc. Effects of Aerobic Physical Exercise on Inflammation and Atherosclerosis in Men:The DNASCO Study:A Six-Year Randomized, Controlled Trial[J]. Annals of Internal Medicine.2004,140(Iss.12),1007-1014.
[12] 傅力.运动与脂代谢的研究进展[J].中国运动医学杂志,1997,16(1)：42-45.
[13] Esposito K, Pontillo A, Di Palo C. Effect of weight loss and lifestyle changes on vascular inflammatory makers in obese women:a randomized trail [J]. JAMA,2003,289(14):1799-1804.
[14] McFarlin BK, Flynn MG, Campbell WW, etc. Physical activity status, but not age, influences inflammatory biomarkers and toll-like receptor 4 [J]. J Gerontol A Biol SciMed Sci,2006, 61(4):388-393.
[15] Kim H, Shin MS, Kim SS, etc. Modulation of immune responses by treadmill exercise in Sprague-Dawley rats [J]. Journal of Sports Medicine and Physical Fitness.2003,43(1): 99-101.
[16] Pacque PFJ, Booth CK, Ball MJ, et al. The effect of an
ultra-endurance running race on mucosal and humoral immune function [J]. Journal of Sports Medicine and Physical Fitness, 2007,47(4):496-501.
[17] 杜丽坤,赵莹,杜立杰,等.实验性糖尿病动物模型的建立[J].现代中西医结合杂志,2004,13(5)：581.
[18] Osorio, R. A., Christofani, J. S., D'Almeida, V., etc. Reactive oxygen species in pregnant rats:effects of exercise and thermal stress [J]. Comp. Biochem. Physiol, Part C Pharmacol. Toxicol.2003,135:89-95.
[19] Fabiano Fernandes da Silva, Renato Aparecido de Souza, Marcos Tadeu Tavares Pacheco,etc. Effects of Different Swimming Exercise Intensities on Bone Tissue Composition in Mice:A Raman Spectroscopy Study [J]. Photomedicine and Laser Surgery,2010:1-9.
[20] Paigen B, Morrow A, Brandon C, etc. Variation in susceptibility to atherosclerosis among inbred strains of mice. Atherosclerosis,1985,57:65-73.
[21]张均田.现代药理实验方法[M].北京：北京医科大学、中国协和医科大学出版社,1998：1263-1271.
[22] 张颖,张波,殷惠军,等.蒺藜总皂苷对家兔高脂血症及主动脉内膜早期粥样硬化病变的影响[J].中西医结合心脑血管病杂志,2006,4(2)：126-147.
[23] 黄霖,李迎新,刘华.实验性糖尿病大鼠动脉粥样硬化模型的建立[J].中国中医急症,2007,16(9)：1111-1113.
[24] Gerrity RG, Natarajan R, Nadler JL, etc. Diabetes-induced acceleraed atherosclerosis in Swine [J]. Diabetes,2001,50(7): 1654-1665.
[25] 王宁,谢自敬,阿布力克木·吐尔地,等.糖尿病大鼠动脉粥样硬化与游离脂肪酸表达的关系[J].中国动脉硬化杂志,2005,13(5)：563-566.
[26] Deboer OJ, Vanderwal AC, Teeling P, etc. Leukocyte recruitment in rupture prone regions of lipid-rich Plaques:a prominent role for neovaseularization [J]. Cardiovas Res,1999, 41:443-449.
[27] Yerneni KK, Bai W, Khan BV, etc. Hyperglycemia-induced activation of nuclear transcription factor kappa B in vaseular smooth muscle cells [J]. Diebetes,1999,48(4):855-864.
[28] Bames pJ, Karin M. Nuclear factor-kappaB:a pivotal transcription factor in chronic inflammatory diseases[J]. N Engl J Med,1997,336(15):1066-1071.
[29] Granet C, Maslinski W, Miossec P, Inereased AP-1 and NF-kaPPaB activation and recruitment with the combination of the Proinflammatory cytokines IL-lbeta, tumor necrosis factor alpha and IL-17 in rheumatoid synoviocytes [J]. Arthritis Res Ther, 2004,6 (3):190-198.
[30] Zhu YM, Bradbury DA, pang L, etc. Transcriptional regulation of interleukin (IL)-8 by bradykinin in human airway smooth muscle cells involves prostanoid-dependent activation of
AP-1 and nuclear factor (NF)-IL-6 and prostanoid-independent activation of NF-kappa B [J]. J Biol Chem,2003,278(31):29366-29375.
[31] Senn JJ, Klover PJ, Nowak IA, et al. Interleukin-6 induces cellular insulin resistance in hepatocytes [J]. Diabetes,2002, 51(12):3391-3399.
[32] Hotamisligil GS. Inflammatory pathways and.insulin action [J]. Int J Obes Relat Metab Disord,2003,27(3):S53-55.
[33] Sunsaneevithayakul P, Boriboohirunsarn D, Sutanthavibul A, etc. Risk factor-based selective screening program for gestational diabetes mellitus in Siriraj Hospital:result from clinical practice guideline [J]. J Med Assoc Thai,2003,86 (8):708-714.
[34] 邹宇峰,蒋晓真,江泉,等.2型糖尿病亚临床大血管病变患者的血清炎症因子变化.内科理论与实践[J],2010,5(4)：319-322.
[35] Libby P, Ridker PM. Inflammation and atherothrombosis:from population biology and bench research to clinical practice. J Am College Cardiol,2006,48(9):33246.
[36] Hojo Y, Ikeda U, Katsuki T, etc. Interleukin 6 expression in coronary circulation after coronary as a risk factor for restenosis. Heart,2000,84:83-87.
[37] Romano M, sironi M, Toniatti C, etc. Chronic treatment with interleukin-1βinduces coronary intimal lesions and vasospa-stic responses in pigs in vivo[J]. Immunity,1997,
6(3):315-325.
[38] Schieffer B, Schieffer E, Hilfiker-Kleiner D. Expression of angiotensin and interleukin 6 in human coronary atherosc-lerotic plaques:Potential implications for inflammation and plaque instability[J]. Circulation,2000,101:1372-1378.
[39] Qin B,Anderson RA, A deliK. Tumor necrosis factor-di rectly stimulates the overproduction of hepatic apolipoprote in B100-containing VLDL via impairment of hepatic insulin signaling [J]. Am J Physiol G astrointest Liver Physiol, 2008,294:G 1120-1129.
[40] Rizvi AA. Inflammation markers as mediators of vasculo endothelial dysfunction and atherosclerosis in the metabolic syndrome[J]. Chin Med J (Engl),2007,120(21):1918-1924.
[41] K leemann R, Zadelaar S, Kooistra T. Cytokines and atherosclerosis:a comprehensive review of studies in mice[J]. Cardiovasc Res,2008,79(3):360-376.
[42] Popa C, Netea MG, van Riel PL, etc. The role of TNF-alpha in chronic inflammatory conditions, intermediary metabolism, and cardiovascular risk[J]. J Lipid Res,2007,48(4):751-762.
[43] Zhang H, Park Y, Wu J, etc. Role of TNF-alpha in vascular dysf unction[J]. Clin Sci(Lond),2009,116(3):219-2130.
[44] 范乐明.动脉粥样硬化炎症机制的再认识[J].中国动脉粥样硬化杂志,2005,13(3)：249-253.
[45] Catheart MK. Regulation of superoxide anion production by
NADPH oxidase in monoeytes/maerophages coniributions to atheroselerosis [J]. Arterioseler Thramb Vase Biol,2004,24(1): 23-28.
[46] 叶建红,李志臻,李众等.代谢综合征患者血清白介素-10与胰岛素抵抗的关系[J].南方医科大学学报,2006,26(4)：428-430.
[47] 李铁,2型糖尿病血型清白介素-10与颈动脉内中膜厚度的相关性研究.硕士学位论文,中国医科大学,2009.
[48] EsPosito K, Ponti110 A, Giugliano F, etc. Assoeiation of 10w-interleukin-10 levels with the metabolic syndrome in Obese women[J]. J Clin Endoerinol Metab,.2003,88(3):1055-1058.
[49] Manigrasso MR, Ferroni P, Santili F, etc. Association between circulating adiponectin and interleukin-10 levels in android obesity:effects of weight loss[J]. J Clin Endoerinol Metab,2005,90(10):5876-5879.
[50] 王飞,戴亚蕾,徐婷等.LPS和IL-10对低密度脂蛋白诱导泡沫细胞形成的影响[J].同济大学学报(医学版),2007,28(1)：1-5.
[51] 王彩丽,魏枫,史平,等.慢性炎症反应对慢性肾功能衰竭患者并发症的影响.放射免疫学杂志,2006,19(1)：18-21.
[52] 朱焕亮,季伟峰,程雅洁.血清CRP, TNF-a, IL-6的水平与颈动脉粥样硬化症的关系.放射免疫学杂志[J],2011,24(1)：110-111.
[53] 杨建斌.不同运动强度对大鼠学习记忆能力及海马细胞凋亡的影响,硕士学位论文,东北师范大学,2009.
[54] 关宇光,李俊平,谢业琪,等.有氧运动对大鼠动脉粥样硬化发生发展过程中血浆CGRP, AngⅡ的影响.沈阳体育学院学报[J].2004,
23(3)：341-343.
[55] 许柳青,叶琼,吴可贵.P38MAPK与血管重构[J].高血压杂志,2005,13：262-265.
[56] 吴诩馨,张海平,李秋萍.有氧运动对高胆固醇血症小鼠血浆内皮素及血脂的影响[J].沈阳体育学院学报,2006,25(4)：50-51.
[57] 柏建清,张云丽,李海军.有氧运动和饮食对脂蛋白代谢及动脉粥样硬化的影响[J].辽宁体育科技,2003,25(1)：26-28.
[58] 胡江亭,张蕴琨.有氧运动对高脂饮食大鼠动脉粥样硬化形成的影响-血清hs-CRP和脂代谢的变化[J].中国运动医学杂志,2006,25(5)：530-533.
[59] 唐植辉,汪南平,钱煦.血流剪切力在动脉粥样硬化形成中的作用书[J].生理科学进展,2007,38(1)：37-41.
[60] 钱芳,周彩萍,康俊芳.运动疗法对糖尿病慢性血管并发症的作用[J].全科医学临床与教育,2011,9(3)：334-337.
[61] 刘善云,何玉秀,张洪侠.耐力训练对ApoE-/-小鼠AS形成及病理变化的干预作用研究.中国运动医学杂志,2011,30(1)：42-52.
[62] Pynn M, Schafer K, Konstantinides, et al. Exercise training reduces neointimal growth and stabilizes vascular lesions developing after injury in apoliprotein e-deficient mice[J]. Circulation,2004,109(3):386-92.
[63] Niebauer J, Maxwell AJ, Lin PS, et al. NOS inhibition accelerates atherogenesis:reversal by exercise [J]. Am J Physiol Heart Circ Physiol,2003,285:H535-H540.
[64] Cesari M, Penninx BS, Pahor M, etc. Inflammatory markers
and physical performance in older persons:the InCHIANTI study[J]. J Gerontol Biol Sci Med Sci,2004,59A:242-248.
[65] 刘善云.耐力训练影响ApoE/—小鼠炎症因子表达与AS防治机制研究.博士学位论文,河北师范大学,2008.
[66] Elosua R, Bartali B, Ordovas J M, etc. Association between physical activity, physical performance, and inflammatory biomarkers in an elderly population:the InCHIANTI study [J]. J Gerontol A Biol Sci Med Sci,2005,60(6):760-767.
[67] Anne Marie W, Petersen, Bente Klarlund Pedersen. The anti-inflammatoy effect of exercise [J]. J AppI Physiol,2005, 98:1154-1162.
[68] 张荣健.飞行员临届高血压患者TNF, SIL-2R NK细胞活性变化的临床意义[J].中国疗养医学,2001(5)：79-80.
[69] Straczkkowski M, Kowalska 1, Dzierfis-Straczkowsko S, etc.Changes in tumor necrosis factor-alpha syslem and sensitivity during an exercise training program in obese women with normaland impaired glucose tolerance[J]. Eud Endoctnol, 2001,145:273-280.
[70] 吴军发吴毅胡永善.运动对OLETF大鼠血清肿瘤坏死因子的影响[J].中华物理医学与康复杂志,2003,25(3)：136-139.
[71] 袁海平,刘学,史仍飞.大鼠不同强度运动对心肌细胞凋亡及其抗氧化能力的影响[J].体育科学,2002,22(1)：107-109.
[72] Davies K J, Quintanilha A T, Brooks G A, Packer L. Free radicals and tissue damage produced by exercise [J].1982.
[73] 吕荣,姜文凯.神经-肌肉疲劳的生理学研究进展[J].2001.
[74] 李为为,渐进性训练对糖尿病大鼠TNF-a和SOD含量的影响.硕士研究生论文,华东师范大学,2006.
[1] Ross R. Atherosclerosis an inflammatory disease[J].N Engl Med, 1999,340:115-126.
[2] Sunsaneevithayakul P, Boriboohirunsarn D, Sutanthavibul A, etc. Risk factor-based selective screening program for gestational diabetes mellitus in Siriraj Hospital:result from clinical practice guideline[J]. J Med Assoc Thai,2003,86(8):708-714.
[3] 吴伟华,张巾超,于江波,等.2型糖尿病及合并大血管病变糖尿病患者C反应蛋白水平观察[J].中华内分泌代谢杂志2003,19(4)：257-259.
[4] Barzilay JI, Abraham L, Heckbert SR, etc. The relation of markers of inflammation to the development of glucose disorders in the elderly:the Cardiovascular Health Study [J]. Diabetes,2001,50(10): 2384-2389.
[5] 李旭光,魏瑞全,李彤,等.2型糖尿病及其伴大血管并发症患者血清IL-6、TNF-a和CRP水平变化[J].西北国防医学杂志,2003,24(3)：219-220.
[6] 李秀钧,邬云红.糖尿病是一种炎症性疾病?[J].中华内分泌代谢杂志,2003,19(4)：251-253。
[7] Esposito K, Pontillo A, Di Palo C. Effect of weight loss and lifestyle changes on vascular inflammatory makers in obese women: a randomized trail [J]. JAMA,2003,289(14):1799-1804.
[8] McFarlin BK, Flynn MG, Campbell WW, etc. Physical activity status, but not age, influences inflammatory biomarkers and toll-like receptor 4 [J]. J Gerontol A Biol SciMed Sci,2006,61(4):388-393.
[9] Pickup J C, Mattock M B, Chusney G D, etc. NIDDM as a disease of the innate immune system:association of acute reactants and intefleukin-6 with metabolic syndrome X[J]. Diabetologia,1997,40: 1286-1292.
[10] Pradhan A D, Manson I E, Nader R, etc. C-reactive protein, interleukin-6, and risk of developing type 2 diabetes mellitus [J]. JAMA,2001,286:327-334.
[11] Freeman D J, Norrie J, Caslake M J, etc. C-reactive protein is an independent predictor of risk for the development of diabetes in the west of Scotland coronary prevention study [J]. Diabetes, 2002,51:1596-1600.
[12] Sen R, Baltimore D. Multiple nuclear factors interact with the immunoglobulin enhancer sequences[J]. Cell,1986,46(5):705.
[13] Viatour P. Mervilk MP. Boufs V, etc. Phosphorylation of NFKB and 1KB proteins, Implications in cancer and inflammation[J]. Trends Blochem sci,2005,30(1):143-52.
[14] Martin Ventura JL, Blanco Colio LM, MunozG arciaB, etc. NF-kappaB activation and Fas ligand overexpression in blood and plaques of patients with carotid atherosclerosis:potential implication in plaque instability[J]. Stroke,2004,35:458-463.
[15] Ho E, Bray TM. NF-kB activation and diabetogenesis[J]. Soc Exp Biol Med,1999,222(3):205-213.
[16] Morigi M, Angioletti S, Imberti B, etc. Leucocyte-endothelial interaction is augmented by high glucose concentrations and
hyperglycemia in a NF-kappa B dependent fashion[J]. J Clin Invest, 1998,101(9):1905-1915.
[17] Yerneni KK, Bai W, Khan BV, etc. Hyperglycemia-induced activation of nuclear transcription factor kappa B in vascular smooth muscle cells [J]. Diabetes,1999,48(4):855-864.
[18] Monaco C, Andreakos E, Kiriakidis S, etc. Canonical pathway of nuclear factor kappa B activation selectively regulates pro-inflammatory and prothrombotic responses in human atherosclerosis [J]. Proc Nail Acad Sci USA,2004,101(15):5634-5639.
[19] MARK A, FEBBRAIO, BENTE KLARLUND PEDERSEN. Muscle-derived interleukin-6:mechanisms for activation and possible biological roles[J]. The FASEB Journal.2002,16:1335-1347.
[20] Hojo Y, Ikeda U, Katsuki T, etc. Interleukin-6 expression in coronary circulation after coronary angioplasty as a risk for restenosis. Heart,2000,84:83-87.
[21] Alexandraki K, PiperiC, KalofoutisC, etc. Inflammatory process in type 2 diabetes:the role of cytokines[J]. Ann N Y Acad Sci,2006, 1084(1):89-117.
[22] Anderon JL, Caripulst JF, Muhlesteln JB, etc. Evalution of Creactive protein, an inflammatory marker and infection serology as risk factor for coronary artery disease and myocardial infarction [J].J Am Coil Candol.1998,3235-38.
[23] Rega G, Kaun C, Weiss TW, etc. Inflammatory cytokines interleukin-6 and oncostatin minduce plasminogen activator
inhibitor-1 in human adipose tissue [J]. Circulation,2005; 111(15) 1938-1945.
[24] Schieffer B, Schieffer E, Hilfiker-kleiner D, etc. Expression of angiotensin Ⅱ and interleukin-6 in human coronary atherosclerotic plaques:potential implications for in flammation and plaque instability[J]. Circulation,2000,101(12):1372-1378.
[25] Antoniades C, TousoulisD, Tountas C, etc. Vascular endothelium and inflammatory process, in patients with combined type 2 diabetes mellitus and coronary atherosclerosis:the effects of vitamin c[J]. Diabet Med,2004; 21(6):552-8.
[26] 刘英晓,王立,休双玲.IL-6与2型糖尿病大血管病变的相关性[J].中国老年医学杂志,2010,9(30)：2513-2515.
[27] K leemann R, Zadelaar S, Kooistra T. Cytokines and atherosclerosis:a comprehensive review of studies in mice[J]. Cardiovasc Res,2008,79(3):360-376.
[28] ZhangH, ParkY, Wu J, etc. Role of TNF-alpha in vascular dysfunction. Clin sci(Lond),2009,116(3):2119-2130.
[29] 高瑞利,张国华.IL-10与动脉硬化性脑缺血性脑卒中[J].脑与神经疾病杂志,2010,18(2)：158-162.
[30] Fuch AC, Granowitz EV, Shapird L, etc. J Clin Immunol,1996, 16:291-303.
[31] Clarkson AN, Liu H, Schiborra F, etc. Angiogenesis as a predictive marker of neurological outcome following hypoxia-ischemia[J]. Brain Res,2007,1171:111-121.
[32] 唐植辉,汪南平,钱煦.血流剪切力在动脉粥样硬化形成中的作用书[J].生理科学进展,2007,38(1)：37-41.
[33] Cesari M, Penninx BS, Pahor M, etc. Inflammatory markers and physical performance in older persons:the InCHIANTI study[J]. J Gerontol Biol Sci Med Sci,2004,59A:242-248.
[34] Christian P. Fischer, Peter Plomga, etc. Endurance training reduces the contraction-induced interleukin-6 mRNA expression in human skeletal muscle[J]. Am J Physiol Endoerinol Metab,2004,287: E1189-1194,
[35] 刘善云.耐力训练影响ApoE小鼠炎症因子表达与AS防治机制研究.博士学位论文,河北师范大学,2008.
[36] 林枫.耐力训练对STZ诱导糖尿病大鼠背根神经节内NF-kB活性的调节作用。硕士毕业论文,南京医科大学,2005。
[37] Vider J, Laaksonen DE, KilK A, etc. Physical exercise induces activation of NF-kappa B in human peripheral blood lymphocytes [J]. Antioxid Redox Singal 2001,3(6):1131-1137.
[38] Hollander J, Fiebig R, Goer M, etc. Superoxide dismutase gene expression is activated by a single bout of exercise in rat skeletal muscle [J]. Pflugers Acrh 2001,442 (3):426-434.
[39] Elosua R, Bartali B, Ordovas J M, etc. Association between physical activity, physical performance, and inflammatory biomarkers in an elderly population:the InCHIANTI study [J]. J Gerontol A Biol Sci Med Sci,2005,60(6):760-767.
[40] Anne Marie W, Petersen, Bente Klarlund Pedersen. The anti-
inflammatoy effect of exercise [J]. J AppI Physiol,2005,98:1154-1162.
[41] 张栩.有氧运动对动脉粥样硬化斑块易损性及基质金属蛋白酶,IL-6水平的影响.博士毕业论文,山东大学,2011。
[42] Straczkkowski M, Kowalska 1, Dzierfis-Straczkowsko S, etc. Changes in tumor necrosis factor-alpha syslem and sensitivity during an exercise training program in obese women with normaland impaired glucose tolerance[J]. Eud Endoctnol,2001,145:273-280.
[43] 吴军发,吴毅,胡永善,等.运动对OLETF大鼠血清肿瘤坏死因子的影响.中华物理医学与康复杂志,2003,(25)3：136-139.
[44] Nara M, Kanda T. Running exercise increases tumor necrosis factor-alpha secreting from mesenteric fat in insulin-resistant rats. Life Sci,1999,65:237-244.
[45] 张荣健.飞行员临届高血压患者TNF, SIL-2R NK细胞活性变化的临床意义[J].中国疗养医学,2001(5)：79-80.
[46] Nieman DC, Henson DA, Smith LL, etc. Cytokine changes after amarathon race[J].J. Appl Physiol,2001,91:109-114.
[47] 唐选.有氧运动预干预对酒精灌胃小鼠肝功能、MDA、IL-10等指标的影响.硕士毕业论文,河南大学,2011.
[48] 孙皓,郭富强,王多姿.运动训练对脑出血大鼠脑组织中IL-10和caspase-3表达的影响[J].中国康复医学,2009,24(9)：783-786。
[49] Nieman DC, Henson DC, Davis JM, etc. Blood leukocyte mRNA expression for IL-10, IL-1Ra, and IL-8, but not IL-6, increases after exercise[J]. Interferon Cytokine Res,2006,26(9):668-674.
[50] 杜厚伟,刘楠,陈荣华.康复训练对脑缺血大鼠神经功能恢复和脑组织中白介素10含量变化的影响[J]。中华物理医学与康复杂志,2006,28(3)：149-152.
[51] 欧阳迎春,王艳,刘应才.6min步行试验对心力衰竭患者细胞因子水平的影响[J].四川医学,2009,30(5)：655-656.
[52] 陈英松,卢峻,吴七柱.艾灸对疲劳模型大鼠血清IL-6和IL-10的影响[J].山东中医杂志,2008,27(6)：404-405.
[2] Ross R. Atherosclerosis-An inflammatory disease[J]. New Engl J Med.1999,340(2):115-216.
[3] 范乐明.动脉粥样硬化炎症机制的再认识[J].中国动脉粥样硬化杂志,2005,13(3)：249-253.
[4] Catheart MK. Regulation of superoxide anion production by NADPH oxidase in monocytes/macrophages coniributions to atherosclerosis[J]. Arterioseler Thramb Vase Biol,2004,24 (1):23-28.
[5] Maiti R, Agrawal N. Atherosclerosis in diabetes mellitus: Role of inflammation [J]. Indian J Med Sci.2007,61(5):292-305.
[6] Sunsaneevithayakul P, Boriboohirunsarn D, Sutanthavibul A, etc.Risk factor-based selective screening program for gestational diabetes mellitus in Siriraj Hospital:result from clinical practice guideline[J]. J Med Assoc Thai,2003,86(8) 708-714.
[7] 吴伟华,张巾超,于江波,等.2型糖尿病及合并大血管病变糖尿病患者C反应蛋白水平观察[J].中华内分泌代谢杂志,2003,19(4)：257-259.
[8] Barzilay JI, Abraham L, Heckbert SR, etc.The relation of markers of inflammation to the development of glucose disorders in the elderly:the Cardiovascular Health Study [J]. Diabetes,
2001,50(10)：2384-2389.
[9] 郭立新.血脂异常与动脉粥样硬化的研究进展[J].世界医学杂志,2002,11(6)：42-44.
[10] 杨永宗.动脉粥样硬化性心血管病基础与临床[M].北京：科学出版社,2004.
[11] Rauramaa R, Halonen P, Vaisanen SB, etc. Effects of Aerobic Physical Exercise on Inflammation and Atherosclerosis in Men:The DNASCO Study:A Six-Year Randomized, Controlled Trial[J]. Annals of Internal Medicine.2004,140(Iss.12),1007-1014.
[12] 傅力.运动与脂代谢的研究进展[J].中国运动医学杂志,1997,16(1)：42-45.
[13] Esposito K, Pontillo A, Di Palo C. Effect of weight loss and lifestyle changes on vascular inflammatory makers in obese women:a randomized trail [J]. JAMA,2003,289(14):1799-1804.
[14] McFarlin BK, Flynn MG, Campbell WW, etc. Physical activity status, but not age, influences inflammatory biomarkers and toll-like receptor 4 [J]. J Gerontol A Biol SciMed Sci,2006, 61(4):388-393.
[15] Kim H, Shin MS, Kim SS, etc. Modulation of immune responses by treadmill exercise in Sprague-Dawley rats [J]. Journal of Sports Medicine and Physical Fitness.2003,43(1): 99-101.
[16] Pacque PFJ, Booth CK, Ball MJ, et al. The effect of an
ultra-endurance running race on mucosal and humoral immune function [J]. Journal of Sports Medicine and Physical Fitness, 2007,47(4):496-501.
[17] 杜丽坤,赵莹,杜立杰,等.实验性糖尿病动物模型的建立[J].现代中西医结合杂志,2004,13(5)：581.
[18] Osorio, R. A., Christofani, J. S., D'Almeida, V., etc. Reactive oxygen species in pregnant rats:effects of exercise and thermal stress [J]. Comp. Biochem. Physiol, Part C Pharmacol. Toxicol.2003,135:89-95.
[19] Fabiano Fernandes da Silva, Renato Aparecido de Souza, Marcos Tadeu Tavares Pacheco,etc. Effects of Different Swimming Exercise Intensities on Bone Tissue Composition in Mice:A Raman Spectroscopy Study [J]. Photomedicine and Laser Surgery,2010:1-9.
[20] Paigen B, Morrow A, Brandon C, etc. Variation in susceptibility to atherosclerosis among inbred strains of mice. Atherosclerosis,1985,57:65-73.
[21]张均田.现代药理实验方法[M].北京：北京医科大学、中国协和医科大学出版社,1998：1263-1271.
[22] 张颖,张波,殷惠军,等.蒺藜总皂苷对家兔高脂血症及主动脉内膜早期粥样硬化病变的影响[J].中西医结合心脑血管病杂志,2006,4(2)：126-147.
[23] 黄霖,李迎新,刘华.实验性糖尿病大鼠动脉粥样硬化模型的建立[J].中国中医急症,2007,16(9)：1111-1113.
[24] Gerrity RG, Natarajan R, Nadler JL, etc. Diabetes-induced acceleraed atherosclerosis in Swine [J]. Diabetes,2001,50(7): 1654-1665.
[25] 王宁,谢自敬,阿布力克木·吐尔地,等.糖尿病大鼠动脉粥样硬化与游离脂肪酸表达的关系[J].中国动脉硬化杂志,2005,13(5)：563-566.
[26] Deboer OJ, Vanderwal AC, Teeling P, etc. Leukocyte recruitment in rupture prone regions of lipid-rich Plaques:a prominent role for neovaseularization [J]. Cardiovas Res,1999, 41:443-449.
[27] Yerneni KK, Bai W, Khan BV, etc. Hyperglycemia-induced activation of nuclear transcription factor kappa B in vaseular smooth muscle cells [J]. Diebetes,1999,48(4):855-864.
[28] Bames pJ, Karin M. Nuclear factor-kappaB:a pivotal transcription factor in chronic inflammatory diseases[J]. N Engl J Med,1997,336(15):1066-1071.
[29] Granet C, Maslinski W, Miossec P, Inereased AP-1 and NF-kaPPaB activation and recruitment with the combination of the Proinflammatory cytokines IL-lbeta, tumor necrosis factor alpha and IL-17 in rheumatoid synoviocytes [J]. Arthritis Res Ther, 2004,6 (3):190-198.
[30] Zhu YM, Bradbury DA, pang L, etc. Transcriptional regulation of interleukin (IL)-8 by bradykinin in human airway smooth muscle cells involves prostanoid-dependent activation of
AP-1 and nuclear factor (NF)-IL-6 and prostanoid-independent activation of NF-kappa B [J]. J Biol Chem,2003,278(31):29366-29375.
[31] Senn JJ, Klover PJ, Nowak IA, et al. Interleukin-6 induces cellular insulin resistance in hepatocytes [J]. Diabetes,2002, 51(12):3391-3399.
[32] Hotamisligil GS. Inflammatory pathways and.insulin action [J]. Int J Obes Relat Metab Disord,2003,27(3):S53-55.
[33] Sunsaneevithayakul P, Boriboohirunsarn D, Sutanthavibul A, etc. Risk factor-based selective screening program for gestational diabetes mellitus in Siriraj Hospital:result from clinical practice guideline [J]. J Med Assoc Thai,2003,86 (8):708-714.
[34] 邹宇峰,蒋晓真,江泉,等.2型糖尿病亚临床大血管病变患者的血清炎症因子变化.内科理论与实践[J],2010,5(4)：319-322.
[35] Libby P, Ridker PM. Inflammation and atherothrombosis:from population biology and bench research to clinical practice. J Am College Cardiol,2006,48(9):33246.
[36] Hojo Y, Ikeda U, Katsuki T, etc. Interleukin 6 expression in coronary circulation after coronary as a risk factor for restenosis. Heart,2000,84:83-87.
[37] Romano M, sironi M, Toniatti C, etc. Chronic treatment with interleukin-1βinduces coronary intimal lesions and vasospa-stic responses in pigs in vivo[J]. Immunity,1997,
6(3):315-325.
[38] Schieffer B, Schieffer E, Hilfiker-Kleiner D. Expression of angiotensin and interleukin 6 in human coronary atherosc-lerotic plaques:Potential implications for inflammation and plaque instability[J]. Circulation,2000,101:1372-1378.
[39] Qin B,Anderson RA, A deliK. Tumor necrosis factor-di rectly stimulates the overproduction of hepatic apolipoprote in B100-containing VLDL via impairment of hepatic insulin signaling [J]. Am J Physiol G astrointest Liver Physiol, 2008,294:G 1120-1129.
[40] Rizvi AA. Inflammation markers as mediators of vasculo endothelial dysfunction and atherosclerosis in the metabolic syndrome[J]. Chin Med J (Engl),2007,120(21):1918-1924.
[41] K leemann R, Zadelaar S, Kooistra T. Cytokines and atherosclerosis:a comprehensive review of studies in mice[J]. Cardiovasc Res,2008,79(3):360-376.
[42] Popa C, Netea MG, van Riel PL, etc. The role of TNF-alpha in chronic inflammatory conditions, intermediary metabolism, and cardiovascular risk[J]. J Lipid Res,2007,48(4):751-762.
[43] Zhang H, Park Y, Wu J, etc. Role of TNF-alpha in vascular dysf unction[J]. Clin Sci(Lond),2009,116(3):219-2130.
[44] 范乐明.动脉粥样硬化炎症机制的再认识[J].中国动脉粥样硬化杂志,2005,13(3)：249-253.
[45] Catheart MK. Regulation of superoxide anion production by
NADPH oxidase in monoeytes/maerophages coniributions to atheroselerosis [J]. Arterioseler Thramb Vase Biol,2004,24(1): 23-28.
[46] 叶建红,李志臻,李众等.代谢综合征患者血清白介素-10与胰岛素抵抗的关系[J].南方医科大学学报,2006,26(4)：428-430.
[47] 李铁,2型糖尿病血型清白介素-10与颈动脉内中膜厚度的相关性研究.硕士学位论文,中国医科大学,2009.
[48] EsPosito K, Ponti110 A, Giugliano F, etc. Assoeiation of 10w-interleukin-10 levels with the metabolic syndrome in Obese women[J]. J Clin Endoerinol Metab,.2003,88(3):1055-1058.
[49] Manigrasso MR, Ferroni P, Santili F, etc. Association between circulating adiponectin and interleukin-10 levels in android obesity:effects of weight loss[J]. J Clin Endoerinol Metab,2005,90(10):5876-5879.
[50] 王飞,戴亚蕾,徐婷等.LPS和IL-10对低密度脂蛋白诱导泡沫细胞形成的影响[J].同济大学学报(医学版),2007,28(1)：1-5.
[51] 王彩丽,魏枫,史平,等.慢性炎症反应对慢性肾功能衰竭患者并发症的影响.放射免疫学杂志,2006,19(1)：18-21.
[52] 朱焕亮,季伟峰,程雅洁.血清CRP, TNF-a, IL-6的水平与颈动脉粥样硬化症的关系.放射免疫学杂志[J],2011,24(1)：110-111.
[53] 杨建斌.不同运动强度对大鼠学习记忆能力及海马细胞凋亡的影响,硕士学位论文,东北师范大学,2009.
[54] 关宇光,李俊平,谢业琪,等.有氧运动对大鼠动脉粥样硬化发生发展过程中血浆CGRP, AngⅡ的影响.沈阳体育学院学报[J].2004,
23(3)：341-343.
[55] 许柳青,叶琼,吴可贵.P38MAPK与血管重构[J].高血压杂志,2005,13：262-265.
[56] 吴诩馨,张海平,李秋萍.有氧运动对高胆固醇血症小鼠血浆内皮素及血脂的影响[J].沈阳体育学院学报,2006,25(4)：50-51.
[57] 柏建清,张云丽,李海军.有氧运动和饮食对脂蛋白代谢及动脉粥样硬化的影响[J].辽宁体育科技,2003,25(1)：26-28.
[58] 胡江亭,张蕴琨.有氧运动对高脂饮食大鼠动脉粥样硬化形成的影响-血清hs-CRP和脂代谢的变化[J].中国运动医学杂志,2006,25(5)：530-533.
[59] 唐植辉,汪南平,钱煦.血流剪切力在动脉粥样硬化形成中的作用书[J].生理科学进展,2007,38(1)：37-41.
[60] 钱芳,周彩萍,康俊芳.运动疗法对糖尿病慢性血管并发症的作用[J].全科医学临床与教育,2011,9(3)：334-337.
[61] 刘善云,何玉秀,张洪侠.耐力训练对ApoE-/-小鼠AS形成及病理变化的干预作用研究.中国运动医学杂志,2011,30(1)：42-52.
[62] Pynn M, Schafer K, Konstantinides, et al. Exercise training reduces neointimal growth and stabilizes vascular lesions developing after injury in apoliprotein e-deficient mice[J]. Circulation,2004,109(3):386-92.
[63] Niebauer J, Maxwell AJ, Lin PS, et al. NOS inhibition accelerates atherogenesis:reversal by exercise [J]. Am J Physiol Heart Circ Physiol,2003,285:H535-H540.
[64] Cesari M, Penninx BS, Pahor M, etc. Inflammatory markers
and physical performance in older persons:the InCHIANTI study[J]. J Gerontol Biol Sci Med Sci,2004,59A:242-248.
[65] 刘善云.耐力训练影响ApoE/—小鼠炎症因子表达与AS防治机制研究.博士学位论文,河北师范大学,2008.
[66] Elosua R, Bartali B, Ordovas J M, etc. Association between physical activity, physical performance, and inflammatory biomarkers in an elderly population:the InCHIANTI study [J]. J Gerontol A Biol Sci Med Sci,2005,60(6):760-767.
[67] Anne Marie W, Petersen, Bente Klarlund Pedersen. The anti-inflammatoy effect of exercise [J]. J AppI Physiol,2005, 98:1154-1162.
[68] 张荣健.飞行员临届高血压患者TNF, SIL-2R NK细胞活性变化的临床意义[J].中国疗养医学,2001(5)：79-80.
[69] Straczkkowski M, Kowalska 1, Dzierfis-Straczkowsko S, etc.Changes in tumor necrosis factor-alpha syslem and sensitivity during an exercise training program in obese women with normaland impaired glucose tolerance[J]. Eud Endoctnol, 2001,145:273-280.
[70] 吴军发吴毅胡永善.运动对OLETF大鼠血清肿瘤坏死因子的影响[J].中华物理医学与康复杂志,2003,25(3)：136-139.
[71] 袁海平,刘学,史仍飞.大鼠不同强度运动对心肌细胞凋亡及其抗氧化能力的影响[J].体育科学,2002,22(1)：107-109.
[72] Davies K J, Quintanilha A T, Brooks G A, Packer L. Free radicals and tissue damage produced by exercise [J].1982.
[73] 吕荣,姜文凯.神经-肌肉疲劳的生理学研究进展[J].2001.
[74] 李为为,渐进性训练对糖尿病大鼠TNF-a和SOD含量的影响.硕士研究生论文,华东师范大学,2006.
[1] Ross R. Atherosclerosis an inflammatory disease[J].N Engl Med, 1999,340:115-126.
[2] Sunsaneevithayakul P, Boriboohirunsarn D, Sutanthavibul A, etc. Risk factor-based selective screening program for gestational diabetes mellitus in Siriraj Hospital:result from clinical practice guideline[J]. J Med Assoc Thai,2003,86(8):708-714.
[3] 吴伟华,张巾超,于江波,等.2型糖尿病及合并大血管病变糖尿病患者C反应蛋白水平观察[J].中华内分泌代谢杂志2003,19(4)：257-259.
[4] Barzilay JI, Abraham L, Heckbert SR, etc. The relation of markers of inflammation to the development of glucose disorders in the elderly:the Cardiovascular Health Study [J]. Diabetes,2001,50(10): 2384-2389.
[5] 李旭光,魏瑞全,李彤,等.2型糖尿病及其伴大血管并发症患者血清IL-6、TNF-a和CRP水平变化[J].西北国防医学杂志,2003,24(3)：219-220.
[6] 李秀钧,邬云红.糖尿病是一种炎症性疾病?[J].中华内分泌代谢杂志,2003,19(4)：251-253。
[7] Esposito K, Pontillo A, Di Palo C. Effect of weight loss and lifestyle changes on vascular inflammatory makers in obese women: a randomized trail [J]. JAMA,2003,289(14):1799-1804.
[8] McFarlin BK, Flynn MG, Campbell WW, etc. Physical activity status, but not age, influences inflammatory biomarkers and toll-like receptor 4 [J]. J Gerontol A Biol SciMed Sci,2006,61(4):388-393.
[9] Pickup J C, Mattock M B, Chusney G D, etc. NIDDM as a disease of the innate immune system:association of acute reactants and intefleukin-6 with metabolic syndrome X[J]. Diabetologia,1997,40: 1286-1292.
[10] Pradhan A D, Manson I E, Nader R, etc. C-reactive protein, interleukin-6, and risk of developing type 2 diabetes mellitus [J]. JAMA,2001,286:327-334.
[11] Freeman D J, Norrie J, Caslake M J, etc. C-reactive protein is an independent predictor of risk for the development of diabetes in the west of Scotland coronary prevention study [J]. Diabetes, 2002,51:1596-1600.
[12] Sen R, Baltimore D. Multiple nuclear factors interact with the immunoglobulin enhancer sequences[J]. Cell,1986,46(5):705.
[13] Viatour P. Mervilk MP. Boufs V, etc. Phosphorylation of NFKB and 1KB proteins, Implications in cancer and inflammation[J]. Trends Blochem sci,2005,30(1):143-52.
[14] Martin Ventura JL, Blanco Colio LM, MunozG arciaB, etc. NF-kappaB activation and Fas ligand overexpression in blood and plaques of patients with carotid atherosclerosis:potential implication in plaque instability[J]. Stroke,2004,35:458-463.
[15] Ho E, Bray TM. NF-kB activation and diabetogenesis[J]. Soc Exp Biol Med,1999,222(3):205-213.
[16] Morigi M, Angioletti S, Imberti B, etc. Leucocyte-endothelial interaction is augmented by high glucose concentrations and
hyperglycemia in a NF-kappa B dependent fashion[J]. J Clin Invest, 1998,101(9):1905-1915.
[17] Yerneni KK, Bai W, Khan BV, etc. Hyperglycemia-induced activation of nuclear transcription factor kappa B in vascular smooth muscle cells [J]. Diabetes,1999,48(4):855-864.
[18] Monaco C, Andreakos E, Kiriakidis S, etc. Canonical pathway of nuclear factor kappa B activation selectively regulates pro-inflammatory and prothrombotic responses in human atherosclerosis [J]. Proc Nail Acad Sci USA,2004,101(15):5634-5639.
[19] MARK A, FEBBRAIO, BENTE KLARLUND PEDERSEN. Muscle-derived interleukin-6:mechanisms for activation and possible biological roles[J]. The FASEB Journal.2002,16:1335-1347.
[20] Hojo Y, Ikeda U, Katsuki T, etc. Interleukin-6 expression in coronary circulation after coronary angioplasty as a risk for restenosis. Heart,2000,84:83-87.
[21] Alexandraki K, PiperiC, KalofoutisC, etc. Inflammatory process in type 2 diabetes:the role of cytokines[J]. Ann N Y Acad Sci,2006, 1084(1):89-117.
[22] Anderon JL, Caripulst JF, Muhlesteln JB, etc. Evalution of Creactive protein, an inflammatory marker and infection serology as risk factor for coronary artery disease and myocardial infarction [J].J Am Coil Candol.1998,3235-38.
[23] Rega G, Kaun C, Weiss TW, etc. Inflammatory cytokines interleukin-6 and oncostatin minduce plasminogen activator
inhibitor-1 in human adipose tissue [J]. Circulation,2005; 111(15) 1938-1945.
[24] Schieffer B, Schieffer E, Hilfiker-kleiner D, etc. Expression of angiotensin Ⅱ and interleukin-6 in human coronary atherosclerotic plaques:potential implications for in flammation and plaque instability[J]. Circulation,2000,101(12):1372-1378.
[25] Antoniades C, TousoulisD, Tountas C, etc. Vascular endothelium and inflammatory process, in patients with combined type 2 diabetes mellitus and coronary atherosclerosis:the effects of vitamin c[J]. Diabet Med,2004; 21(6):552-8.
[26] 刘英晓,王立,休双玲.IL-6与2型糖尿病大血管病变的相关性[J].中国老年医学杂志,2010,9(30)：2513-2515.
[27] K leemann R, Zadelaar S, Kooistra T. Cytokines and atherosclerosis:a comprehensive review of studies in mice[J]. Cardiovasc Res,2008,79(3):360-376.
[28] ZhangH, ParkY, Wu J, etc. Role of TNF-alpha in vascular dysfunction. Clin sci(Lond),2009,116(3):2119-2130.
[29] 高瑞利,张国华.IL-10与动脉硬化性脑缺血性脑卒中[J].脑与神经疾病杂志,2010,18(2)：158-162.
[30] Fuch AC, Granowitz EV, Shapird L, etc. J Clin Immunol,1996, 16:291-303.
[31] Clarkson AN, Liu H, Schiborra F, etc. Angiogenesis as a predictive marker of neurological outcome following hypoxia-ischemia[J]. Brain Res,2007,1171:111-121.
[32] 唐植辉,汪南平,钱煦.血流剪切力在动脉粥样硬化形成中的作用书[J].生理科学进展,2007,38(1)：37-41.
[33] Cesari M, Penninx BS, Pahor M, etc. Inflammatory markers and physical performance in older persons:the InCHIANTI study[J]. J Gerontol Biol Sci Med Sci,2004,59A:242-248.
[34] Christian P. Fischer, Peter Plomga, etc. Endurance training reduces the contraction-induced interleukin-6 mRNA expression in human skeletal muscle[J]. Am J Physiol Endoerinol Metab,2004,287: E1189-1194,
[35] 刘善云.耐力训练影响ApoE小鼠炎症因子表达与AS防治机制研究.博士学位论文,河北师范大学,2008.
[36] 林枫.耐力训练对STZ诱导糖尿病大鼠背根神经节内NF-kB活性的调节作用。硕士毕业论文,南京医科大学,2005。
[37] Vider J, Laaksonen DE, KilK A, etc. Physical exercise induces activation of NF-kappa B in human peripheral blood lymphocytes [J]. Antioxid Redox Singal 2001,3(6):1131-1137.
[38] Hollander J, Fiebig R, Goer M, etc. Superoxide dismutase gene expression is activated by a single bout of exercise in rat skeletal muscle [J]. Pflugers Acrh 2001,442 (3):426-434.
[39] Elosua R, Bartali B, Ordovas J M, etc. Association between physical activity, physical performance, and inflammatory biomarkers in an elderly population:the InCHIANTI study [J]. J Gerontol A Biol Sci Med Sci,2005,60(6):760-767.
[40] Anne Marie W, Petersen, Bente Klarlund Pedersen. The anti-
inflammatoy effect of exercise [J]. J AppI Physiol,2005,98:1154-1162.
[41] 张栩.有氧运动对动脉粥样硬化斑块易损性及基质金属蛋白酶,IL-6水平的影响.博士毕业论文,山东大学,2011。
[42] Straczkkowski M, Kowalska 1, Dzierfis-Straczkowsko S, etc. Changes in tumor necrosis factor-alpha syslem and sensitivity during an exercise training program in obese women with normaland impaired glucose tolerance[J]. Eud Endoctnol,2001,145:273-280.
[43] 吴军发,吴毅,胡永善,等.运动对OLETF大鼠血清肿瘤坏死因子的影响.中华物理医学与康复杂志,2003,(25)3：136-139.
[44] Nara M, Kanda T. Running exercise increases tumor necrosis factor-alpha secreting from mesenteric fat in insulin-resistant rats. Life Sci,1999,65:237-244.
[45] 张荣健.飞行员临届高血压患者TNF, SIL-2R NK细胞活性变化的临床意义[J].中国疗养医学,2001(5)：79-80.
[46] Nieman DC, Henson DA, Smith LL, etc. Cytokine changes after amarathon race[J].J. Appl Physiol,2001,91:109-114.
[47] 唐选.有氧运动预干预对酒精灌胃小鼠肝功能、MDA、IL-10等指标的影响.硕士毕业论文,河南大学,2011.
[48] 孙皓,郭富强,王多姿.运动训练对脑出血大鼠脑组织中IL-10和caspase-3表达的影响[J].中国康复医学,2009,24(9)：783-786。
[49] Nieman DC, Henson DC, Davis JM, etc. Blood leukocyte mRNA expression for IL-10, IL-1Ra, and IL-8, but not IL-6, increases after exercise[J]. Interferon Cytokine Res,2006,26(9):668-674.
[50] 杜厚伟,刘楠,陈荣华.康复训练对脑缺血大鼠神经功能恢复和脑组织中白介素10含量变化的影响[J]。中华物理医学与康复杂志,2006,28(3)：149-152.
[51] 欧阳迎春,王艳,刘应才.6min步行试验对心力衰竭患者细胞因子水平的影响[J].四川医学,2009,30(5)：655-656.
[52] 陈英松,卢峻,吴七柱.艾灸对疲劳模型大鼠血清IL-6和IL-10的影响[J].山东中医杂志,2008,27(6)：404-405.
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