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王 雁,任爱华,翁秀妹,章淑萍.运动干预对实验性高同型半胱氨酸血症大鼠过氧化及血管内皮功能的影响[J].中国康复医学杂志,2016,(11):1208~1212
运动干预对实验性高同型半胱氨酸血症大鼠过氧化及血管内皮功能的影响    点此下载全文
王 雁  任爱华  翁秀妹  章淑萍
浙江医院心脏康复中心,杭州灵隐路12号,310013
基金项目:浙江省自然科学基金资助项目(LY12H17001)
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摘要:
      摘要 目的:探讨运动干预对实验性高同型半胱氨酸血症(hyperhomocysteinemia, HHcy)大鼠过氧化及血管内皮功能的影响。 方法:将48只大鼠随机分为6组,每组各8只。对照组(n=8只)给予普通饲料喂养;高蛋氨酸组(n=40只)在此基础上加3%的蛋氨酸,再根据运动强度分为模型组、叶酸组、HHcy运动组(低强度组、中强度组、高强度组),8只/组,持续16周。检测各组大鼠血清同型半胱氨酸(Hcy)、血浆丙二醛(MDA)含量和谷胱甘肽过氧化物酶(GSH-PX)、超氧化物歧化酶(SOD)活性,测定一氧化氮(NO)、一氧化氮合酶(NOS)、内皮素1(ET-1)水平。 结果:干预后8周,HHcy运动组血清Hcy水平明显下降,且显著低于模型组(16.09±4.85 vs. 24.24±3.11μmol/L)(P<0.05);干预后16周,HHcy运动组血清Hcy水平与对照组无显著性差异(7.81±0.64 vs. 6.63±1.27μmol/L)(P>0.05),各组血清Hcy水平依次为叶酸组(6.63±1.27μmol/L)>低强度组(7.62±0.73μmol/L)>中强度组(6.91±0.37μmol/L)>高强度组(6.19±0.34μmol/L)(P<0.05);干预后16周,HHcy运动组MDA均显著下降,SOD活力和GSH-PX含量明显升高(P<0.05),中、高强度运动组各过氧化指标与对照组无显著性差异(P>0.05);与对照组比较,干预后16周模型组、叶酸组和低强度组ET-1明显升高(61.64±12.29、58.86±10.32、59.11±9.09 vs 49.48±11.09 pg/ml),NOS(8.52±2.09、18.13±4.65、17.08±4.20 vs 33.98±6.67U/ml)、NO(1.19±0.24、1.30±0.41、1.30±0.41 vs 2.29±0.28μg/L)明显下降(P<0.05),而中强度组、高强度组中ET-1、NOS与对照组比较,差异无显著性意义(P>0.05);HHcy运动组、叶酸组NO均明显高于模型组(P<0.05)。 结论:高蛋氨酸饮食可诱发大鼠HHcy,而中、高强度运动干预有助于降低HHcy大鼠血清Hcy水平,改善氧化应激状态,减轻内皮功能损伤。
关键词:运动干预  高同型半胱氨酸血症  动脉粥样硬化  过氧化  血管内皮功能
Influence of exercise intervention on peroxidation and vascular endothelial function for experimental hyperhomocysteinemia rats    Download Fulltext
Dept. of Cardiac Rehabilitation, Zhejiang Hospital, Hangzhou, 310013
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Abstract:
      Abstract Objective: To explore the influence of exercise intervention on peroxidation and vascular endothelial function for experimental hyperhomocysteinemia (HHcy) rats. Method: Forty-eight male rats were randomly and equally divided into six groups. Control group (n=8) was given with ordinary feed. Being fed with 3% methionine on this basis, high methionine group (n=40) was divided into model group, folic acid group, HHcy exercise group (low intensity group, middle intensity group and high intensity group)(8 rats per group for 16 weeks intervention)according to exercise intensity. Serum homocysteine (Hcy), content of plasma malondialdehyde (MDA), activity of glutathione peroxidase (GSH-PX) and superoxide dismutase (SOD) were detected, and the level of nitric oxide (NO), nitric oxide synthase (NOS), endothelin 1 (ET-1) was measured. Result: At 8 weeks after intervention, the level of serum Hcy in the HHcy exercise group was significantly reduced, and lower than that in the model group (16.09±4.85 vs. 24.24±3.11μmol/L) (P<0.05). At 16 weeks after intervention, the level had no significant difference when compared with the control group (7.81±0.64 vs. 6.63±1.27μmol/L) (P>0.05). The level of serum Hcy was in this order: folic acid group (6.63±1.27μmol/L) > low intensity group (7.62±0.73μmol/L) > middle intensity group (6.91±0.37μmol/L) > high intensity group (6.19±0.34μmol/L) (P<0.05). At 16 weeks after intervention, the content of MDA in the HHcy exercise group was reduced, and activity of SOD and GSH-PX was increased (P<0.05). There were no significant difference on the peroxide index between the middle and high intensity group compared with the control group (P>0.05). Compared with the control group, the level of ET-1 in the model group, folic acid group and low intensity group was increased (61.64±12.29, 58.86±10.32, 59.11±9.09 vs 49.48±11.09pg/ml), and the level of NOS (8.52±2.09, 18.13±4.65, 17.08±4.20 vs 33.98±6.67U/ml) and NO (1.19±0.24, 1.30±0.41, 1.30±0.41 vs 2.29±0.28μg/L) was reduced (P<0.05), while there was no significant difference on the the level of NOS and NO between middle intensity group, high intensity group and control group (P>0.05). The levels of NO in the HHcy exercise group and folic acid group were significantly higher than those in the model group (P<0.05). Conclusion: High methionine diet can induce HHcy in rats, and middle and high intensity exercise intervention can reduce the level of serum Hcy, improve oxidative stress state, and reduce the injury of endothelial function.
Keywords:exercise intervention  hyperhomocysteinemia  atherosclerosis  peroxidation  vascular endothelial function
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