急性力竭运动大鼠肾组织总抗氧能力及自由基代谢的变化

目的:观察大鼠在安静、急性力竭运动中、运动力竭即刻和恢复24h四种功能状态,肾组织总抗氧能力及丙二醛含量的变化。方法:实验于2005-10在曲阜师范大学体育科学学院生化实验室完成。①选用成年雄性Wistar大鼠32只。随机分为4组:安静对照组、游泳40min组、力竭即刻组和恢复24h组,每组8只。各组大鼠均进行2d适应性游泳。第3天,安静对照组大鼠不游泳直接取材;其余组大鼠尾部负重3%体质量的铅条游泳,不断用铁棒搅动迫使大鼠游动。游泳40min组、力竭即刻组和恢复24h组大鼠在游泳40min后、力竭运动后即刻、力竭运动后24h取材。力竭标准:大鼠沉入水面下10s,托起后再次沉下,反复两三次,视为力竭。②按南京建成生物工程研究所试剂盒说明进行操作测定肾组织总抗氧能力、丙二醛含量。③计量资料差异比较采用t检验。结果:纳入大鼠32只,均进入结果分析,无脱失值。①肾组织总抗氧能力:游泳40min组、力竭即刻组分别为(3.63±0.64),(3.65±0.99)kU/g,高于安静对照组[(2.99±0.17)kU/g,P<0.05);力竭即刻组略高于游泳40min组,但差异不明显(P>0.05);恢复24h组为(2.96±0.67)kU/g,略低于安静对照组,差异也不明显(P>0.05)。②肾组织丙二醛含量:游泳40min组、力竭即刻组分别为(4.38±1.34),(4.74±1.65)μmol/g,高于安静对照组[(3.45±0.28)μmol/g,P<0.05,0.01];力竭即刻组高于游泳40min组,但差异不明显(P>0.05)。恢复24h状态,达到最大值为(7.66±1.52)μmol/g,高于其他3组(P<0.01)。结论:急性力竭运动大鼠肾组织内抗氧化能力和丙二醛含量较安静状态时提高,力竭运动后24h总抗氧化能力恢复至安静状态水平,丙二醛含量仍高。     

糖尿病大鼠骨骼肌细胞膜葡葡糖转运蛋白4含量在不同强度运动状态下的变化

背景:运动能影响骨骼肌细胞膜葡萄糖转运蛋白4含量,但不同强度的运动对骨骼肌细胞膜葡萄糖转运蛋白4含量产生怎样的影响还不被人们所知.目的:拟了解不同强度运动对大鼠骨骼肌细胞膜葡萄糖转运蛋白4含量的影响.设计、时间及地点:随机对照动物实验,于2007-09/10在辽宁师范大学中心实验室完成.材料:健康SD大鼠60只,体质量(200±16)g,雌雄不拘.方法:制备糖尿病大鼠模型.将SD大鼠分为6组:正常对照组、糖尿病对照组和糖尿病4种不同强度运动组(包括15m/min组、20m/min组、25m/min组和30m/min组),每组10只.运动组按上述强度训练50min/d, 6d/周,共6周.主要观察指标:用Western blot免疫印迹法检测骨骼肌细胞膜表面葡萄糖转运蛋白4表达:并观察不同强度运动对各组大鼠体质量、血糖和胰岛素水平的影响.结果:①与糖尿病对照组相比,20m/min和25m/min组股四头肌葡萄糖转运蛋白4含量分别升高44.2%和48.0%(P＜0.01);15m/min和30m/min组股四头肌葡萄糖转运蛋白4含量分别升高17.3%和19.2%(P＜0.05),但各组仍没有恢复到正常对照组水平.②与糖尿病对照组相比,20m/min组大鼠体质量恢复良好(P＜0.05);不同强度运动组大鼠血糖均下降(P＜0.05或P＜0.01),以15m/min组和20m/min组下降显著;15m/min组、20m/min组和25m/min组大鼠胰岛素水平均显著升高(P＜0.01).结论:以20m/min和25m/min的强度运动对SD大鼠股四头肌葡萄糖转运蛋白4含量的升高可能具有最佳的影响效果.     

染料木黄酮对幼年大鼠脂代谢和抗氧化作用的影响

目的:染料木横酮是大豆异黄酮的主要成分之一.目前,有关大豆黄酮对脂代谢及抗氧化方面的研究对象主要是成年动物,它对幼年大鼠是否也具有类似效应,实验观察染料木黄酮对幼年大鼠脂类代谢和抗氧化作用的影响.方法:实验于2006-10/12在南京农业大学动物医学院生物化学教研室完成.①实验材料:21日龄清洁级幼年期雄性SD大鼠20只,体质量为(85±5) g;染料木黄酮(Sigma公司),纯度>99%,制成5 g/L的受试液备用.②实验分组及过程:将SD大鼠随机平均分为2组,实验组腹腔注射 5 mg/kg体质量的染料木黄酮,对照组腹腔注射体积分数为0.5的乙醇 体积分数为0.5的丙二醇混合液,隔天注射1次,连续7次.③实验评估:两组幼年期大鼠腹脂率、生化指标及内分泌激素.结果:①腹脂率:染料木黄酮使幼年期大鼠腹脂率降低了6.51%.②生化指标:与对照组相比,试验组大鼠血糖含量升高了60.73%(P＜0.01),血清三酰甘油、总胆固醇、非酯化脂肪酸、胰岛素、肿瘤坏死因子α分别降低了35.62%,22.73%,29.08%(P均 < 0.01)、4.46%(P＞0.05),24.12%(P＜0.01);肝脏中糖原、三酰甘油、总胆固醇的含量分别降低了70.04%,58.91%,和31.19%(P均 < 0.01);脂蛋白脂酶、肝脂酶及总脂酶分别升高了46.51%(P＜0.05),32.35%和42.08%(P＜0.05);琥珀酸脱氢酶、丙酮酸激酶、Na -K -ATPase分别升高了54.39%,86.45%,549.50%(P 均 < 0.01)染料木黄酮处理后大鼠肝脏中超氧化物歧化酶、总抗氧化能力、谷胱甘肽过氧化物酶活性分别较对照组升高了7.07%,53.66%(P＜0.01)和21.72%,丙二醛含量降低了11.54%(P＜0.01).③内分泌激素:与对照组相比,实验组中胰岛素、肿瘤坏死因子α的含量分别降低了4.46%,24.12%(P＜0.01),胰高血糖素的含量升高了12.26%.结论:染料木黄酮具有降低幼年期大鼠血脂和增强抗氧化能力的作用.     

针刺丘脑底核后帕金森病模型大鼠抗氧化能力的变化

背景：针灸在治疗帕金森病的有效性已为临床及实验所证实，但是临床仍缺乏系统、完整、可遵循的治疗原则和规律。 目的：观察针刺丘脑底核对帕金森病大鼠损毁侧纹状体谷胱甘肽、谷胱甘肽过氧化物酶、超氧化物歧化酶、丙二醛、一氧化氮合酶的影响。 设计：随机对照动物实验。 单位：黑龙江中医药大学第二附属医院。 材料：实验于2003-01／06在黑龙江中医药大学实验动物中心实验室进行。取健康清洁级成年Wistar大鼠18只，单纯随机分为3组：电针组、模型组、盐水组，每组6只。 方法：①模型组：将6-羟基多巴（12μg溶于5斗L含2g／L抗坏血酸的生理盐水中）缓慢注入尾壳核，建立纹状体毁损帕金森病大鼠模型，不干预。②盐水组：将6-羟基多巴改为等刺量的生理盐水，其余处理同模型组。③电针组：同模型组造模，术后6周丘脑底核埋针，1周后进行电针治疗（频率为100Hz，强度1mA左右），1次／d，15min／次，连续治疗2周。 主要观察指标：所有大鼠在电针组大鼠电针2周后麻醉状态下断头取脑，比色法检测谷胱甘肽、谷胱甘肽过氧化物酶、超氧化物歧化酶、丙二醛和一氧化氮合酶活性。 结果：18只大鼠进入结果分析。①丙二醛浓度：模型组和电针组均高于盐水组【（5．53&;#177;0．71），（4．10&;#177;0．27），（5．53&;#177;0．71）μmol／L，P〈0．01]，但电针组低于模型组（P〈0．05）。②谷胱甘肽和谷胱甘肽过氧化物酶活性：模型组和电针组均低于盐水组（P〈0．01），但电针组高于模型组（P〈0．05）。③一氧化氮合酶活性：模型组和电针组均高于盐水组【（113．36&;#177;2．17），（73．85&;#177;5．17）。（42．34&;#177;1．83）μkat／g，P〈0．01]，但电针组低于模型．组（P〈0．01）。 结论：针刺后帕金森病模型大鼠抗氧化防御能力得到恢复，神经损伤减轻。说明针刺脑内核团治疗帕金森病的方法是可行的、有效的。     

针刺丘脑底核后帕金森病模型大鼠抗氧化能力的变化

背景:针灸在治疗帕金森病的有效性已为临床及实验所证实,但是临床仍缺乏系统、完整、可遵循的治疗原则和规律。目的:观察针刺丘脑底核对帕金森病大鼠损毁侧纹状体谷胱甘肽、谷胱甘肽过氧化物酶、超氧化物歧化酶、丙二醛、一氧化氮合酶的影响。设计:随机对照动物实验。单位:黑龙江中医药大学第二附属医院。材料:实验于2003-01/06在黑龙江中医药大学实验动物中心实验室进行。取健康清洁级成年Wistar大鼠18只,单纯随机分为3组:电针组、模型组、盐水组,每组6只。方法:①模型组:将6-羟基多巴(12μg溶于5μL含2g/L抗坏血酸的生理盐水中)缓慢注入尾壳核,建立纹状体毁损帕金森病大鼠模型,不干预。②盐水组:将6-羟基多巴改为等剂量的生理盐水,其余处理同模型组。③电针组:同模型组造模,术后6周丘脑底核埋针,1周后进行电针治疗(频率为100Hz,强度1mA左右),1次/d,15min/次,连续治疗2周。主要观察指标:所有大鼠在电针组大鼠电针2周后麻醉状态下断头取脑,比色法检测谷胱甘肽、谷胱甘肽过氧化物酶、超氧化物歧化酶、丙二醛和一氧化氮合酶活性。结果:18只大鼠进入结果分析。①丙二醛浓度:模型组和电针组均高于盐水组[(5.53±0.71),(4.10±0.27),(5.53±0.71)μmol/L,P<0.01],但电针组低于模型组(P<0.05)。②谷胱甘肽和谷胱甘肽过氧化物酶活性:模型组和电针组均低于盐水组(P<0.01),但电针组高于模型组(P<0.05)。③一氧化氮合酶活性:模型组和电针组均高于盐水组[(113.36±2.17),(73.85±5.17),(42.34±1.83)μkat/g,P<0.01],但电针组低于模型组(P<0.01)。结论:针刺后帕金森病模型大鼠抗氧化防御能力得到恢复,神经损伤减轻。说明针刺脑内核团治疗帕金森病的方法是可行的、有效的。     

Structure and function of skeletal muscles

This review describes the structural make-up of muscle cells in term of the organization of the main myo-proteins into sarcomeres. The activation of muscle contraction is discussed on the cellular level as well as an integrative problem of activation of motor units for motor task. In this context the discrimination of muscle fibers into slow and fast types plays a role in particular with regard to specific athletic qualities. The energy supply systems present themselves as a sequence of distinct processes, which are responsible for power output for seconds, (phosphocreatine), minutes (glycolysis) and minutes to hours (oxidative phosphorylation). The supply of oxygen is a limiting condition for continued muscle work as the body does not maintain sizeable stores of oxygen. By contrast substrates (both carbohydrates and lipids) are stored in myocytes as well as systemically and do therefore not represent immediate limits to exercise performance.     

Contractile properties of rat skeletal muscles following storage at 4 degrees C.

The purpose of this study was to assess the potential of preservation solutions for protecting skeletal muscle function during storage at 4 degrees C. The soleus and the cutaneus trunci (CT) from the rat were stored for 2, 8 or 16 h at 4 degrees C in University of Wisconsin solution (UW), HTK-Bretschneider solution (HTK) or Krebs-Henseleit solution (KH). After storage, muscles were stimulated electrically to analyse the isometric contractile properties, such as the maximum tetanic tension (P(0)). Histological analysis was also performed. In separate experiments, the effect of the diffusion distance on muscle preservation was studied by bisecting the soleus. After 8 h of storage in UW or HTK, the contractile properties of the CT were similar to those of the control, whereas those of the soleus were reduced (P(0) values of 16% and 69% of control in UW and HTK respectively). At 16 h, the contractile properties of the CT (P(O) 28%) were again better preserved than those of the soleus (P(0) 9%). Muscle function deteriorated most after storage in KH (P(0) at 16 h: soleus, 3%; CT, 17%). The bisected soleus was equally well preserved as the CT (P(O) of bisected soleus at 8 h in UW and HTK: 86%). The functional data corresponded well with the histological data, which showed increasing muscle fibre derangement with increasing storage time. For both muscles and all solutions, the threshold stimulus current increased with increasing storage time (control, 0.1 mA; 16 h, 1.2 mA) and was strongly correlated with the deterioration in contractile properties. It is concluded that, at 4 degrees C, muscle is preserved better in UW and HTK (intracellular-like solutions) than in KH (extracellular-like solution). The soleus and CT were best protected in HTK. The diffusion distance is a critical factor for successful preservation of muscle function at 4 degrees C. The reduced function after 16 h of storage at 4 degrees C was caused by hypercontraction and necrosis of about 25% of the muscle fibres, and by deterioration of the electrical component of excitation-contraction coupling of the remaining fibres.     

大鼠骨骼肌细胞异柠檬酸脱氢酶和琥珀酸脱氢酶活性在不同训练负荷时的变化

背景：异柠檬酸脱氢酶和琥珀酸脱氢酶是糖有氧氧化过程中的关键酶,不同训练方式和训练时间对骨骼肌异柠檬酸脱氢酶和琥珀酸脱氢酶活性影响的报道较少。目的：探讨不同训练负荷条件对大鼠骨骼肌异柠檬酸脱氢酶和琥珀酸脱氢酶活性的影响。方法：参照BEDFORD TG标准,建立大鼠有氧、无氧和有氧无氧交替运动跑台训练模型,正常饲养的大鼠作为对照。训练结束后,紫外分光光度计检测大鼠骨骼肌异柠檬酸脱氢酶和琥珀酸脱氢酶的活性。结果与结论：有氧运动4,6周,大鼠骨骼肌异柠檬酸脱氢酶和琥珀酸脱氢酶活性均明显升高（P〈0.05）;交替运动2周,异柠檬酸脱氢酶和琥珀酸脱氢酶活性增加（P〈0.05）,运动至4,6周时,两种酶活性均下降（P〈0.05）;而无氧运动对异柠檬酸脱氢酶和琥珀酸脱氢酶活性无影响。结果提示：长期的有氧运动和短时间的有氧无氧交替运动有利于提升骨骼肌异柠檬酸脱氢酶和琥珀酸脱氢酶的活性。     

大鼠骨骼肌细胞异柠檬酸脱氢酶和琥珀酸脱氢酶活性在不同训练负荷时的变化

背景:异柠檬酸脱氢酶和琥珀酸脱氢酶是糖有氧氧化过程中的关键酶,不同训练方式和训练时间对骨骼肌异柠檬酸脱氢酶和琥珀酸脱氢酶活性影响的报道较少。目的:探讨不同训练负荷条件对大鼠骨骼肌异柠檬酸脱氢酶和琥珀酸脱氢酶活性的影响。方法:参照BEDFORD TG标准,建立大鼠有氧、无氧和有氧无氧交替运动跑台训练模型,正常饲养的大鼠作为对照。训练结束后,紫外分光光度计检测大鼠骨骼肌异柠檬酸脱氢酶和琥珀酸脱氢酶的活性。结果与结论:有氧运动4,6周,大鼠骨骼肌异柠檬酸脱氢酶和琥珀酸脱氢酶活性均明显升高(P<0.05);交替运动2周,异柠檬酸脱氢酶和琥珀酸脱氢酶活性增加(P<0.05),运动至4,6周时,两种酶活性均下降(P<0.05);而无氧运动对异柠檬酸脱氢酶和琥珀酸脱氢酶活性无影响。结果提示:长期的有氧运动和短时间的有氧无氧交替运动有利于提升骨骼肌异柠檬酸脱氢酶和琥珀酸脱氢酶的活性。     

Aminoglycoside antibiotics restore dystrophin function to skeletal muscles of mdx mice

Duchenne muscular dystrophy (DMD) is caused by mutations in the dystrophin gene, leading to the absence of the dystrophin protein in striated muscle. A significant number of these mutations are premature stop codons. On the basis of the observation that aminoglycoside treatment can suppress stop codons in cultured cells, we tested the effect of gentamicin on cultured muscle cells from the mdx mouse - an animal model for DMD that possesses a premature stop codon in the dystrophin gene. Exposure of mdx myotubes to gentamicin led to the expression and localization of dystrophin to the cell membrane. We then evaluated the effects of differing dosages of gentamicin on expression and functional protection of the muscles of mdx mice. We identified a treatment regimen that resulted in the presence of dystrophin in the cell membrane in all striated muscles examined and that provided functional protection against muscular injury. To our knowledge, our results are the first to demonstrate that aminoglycosides can suppress stop codons not only in vitro but also in vivo. Furthermore, these results raise the possibility of a novel treatment regimen for muscular dystrophy and other diseases caused by premature stop codon mutations. This treatment could prove effective in up to 15% of patients with DMD.     

Neuropeptide Y induces ischemic angiogenesis and restores function of ischemic skeletal muscles

Previously we showed that neuropeptide Y (NPY), a sympathetic vasoconstrictor neurotransmitter, stimulates endothelial cell migration, proliferation, and differentiation in vitro. Here, we report on NPY's actions, receptors, and mediators in ischemic angiogenesis. In rats, hindlimb ischemia stimulates sympathetic NPY release (attenuated by lumbar sympathectomy) and upregulates NPY-Y2 (Y2) receptor and a peptidase forming Y2/Y5-selective agonist. Exogenous NPY at physiological concentrations also induces Y5 receptor, stimulates neovascularization, and restores ischemic muscle blood flow and performance. NPY-mediated ischemic angiogenesis is not prevented by a selective Y1 receptor antagonist but is reduced in Y2(-/-) mice. Nonischemic muscle vascularity is also lower in Y2(-/-) mice, whereas it is increased in NPY-overexpressing rats compared with their WT controls. Ex vivo, NPY-induced aortic sprouting is markedly reduced in Y2(-/-) aortas and spontaneous sprouting is severely impaired in NPY(-/-) mice. NPY-mediated aortic sprouting, but not cell migration/proliferation, is blocked by an antifetal liver kinase 1 antibody and abolished in mice null for eNOS. Thus, NPY mediates neurogenic ischemic angiogenesis at physiological concentrations by activating Y2/Y5 receptors and eNOS, in part due to release of VEGF. NPY's effectiveness in revascularization and restoring function of ischemic tissue suggests its therapeutic potential in ischemic conditions.     

Effects of short-term electrical stimulation on the ultrastructure of rat skeletal muscles

The purpose of this study was to determine the effects of short-term, 2,500-Hz carrier-wave frequency electrical stimulation on the ultrastructure of fast-twitch rat skeletal muscles. Thirteen Sprague-Dawley male rats were divided into three groups: daily treatment (Group 1), every-other-day treatment (Group 2), and control (Group 3). The medial quadriceps femoris and hamstring (semitendinosus and semimembranosus) muscles of the right thigh were treated with short-term electrical stimulation. After treatment, the animals were sacrificed, and their treated and sham quadriceps femoris and hamstring muscles were removed, fixed by immersion, and processed for electron microscopy. Morphometric measurements were made on electron micrographs using a Videoplan computer system, and the results were analyzed statistically. The results revealed that mitochondria, triads, and glycogen content of the fast-twitch muscles changed to resemble those of slow-twitch muscles. In view of these results, clinicians should consider the possibility that similar changes also might occur in human subjects under clinical conditions.