过表达肌浆网Ca2+-ATP酶对慢性心力衰竭犬神经内分泌系统的影响

目的研究心肌过表达肌浆网Ca2+-ATP酶(SERCA2a)基因对慢性心力衰竭犬神经内分泌系统的影响。方法超声心动图检测SERCA2a基因转导对慢性心力衰竭犬心脏收缩功能的影响,放射免疫法测定血管紧张素Ⅱ与心房利钠肽、内皮素-1、肿瘤坏死因子-α、白介素-6等神经内分泌因子。结果 SERCA2a基因转导后心力衰竭犬的心脏收缩功能得到改善(P<0.05),同时上述神经内分泌因子水平均减低(P<0.05)。结论 SERCA2a过表达能改善心肌收缩功能,阻断神经内分泌系统的恶性循环,可能阻止或逆转心肌重塑。     

骨骼肌肌浆网Na+,K+-ATP酶和Ca2+-ATP酶活性在不同训练条件下的变化

背景:Na+,K+-ATP酶和Ca2+-ATP酶存物质运送、能量转换以及信息传递方面具有重要作用.肌浆网在肌肉兴奋-收缩耦联过程中起关键作用,与运动性骨骼肌疲劳的发生密切关.目的:通过建立SD大鼠有氧和无氧训练模型,观察不同训练负荷条件对大鼠骨骼肌肌浆网Na+,K+-ATP酶和Ca2+-ATP酶活性的影响.方法:参照Bedford TG标准,建立有氧和无氧运动大鼠跑台训练模型,有氧运动组采用递增负荷训练,无氧运动组采用高速间歇训练,正常对照组大鼠正常笼内生活,不运动.各组动物训练结束后用超速离心法提取大鼠骨骼肌肌浆网,紫外分光光度汁检测大鼠骨骼肌肌浆网Na+,K+-ATP酶和Ca2+-ATP酶的活性.结果与结论:训练4周后,两个运动组大鼠骨骼肌肌浆网Na+,K+-ATP酶和Ca2+-ATP酶的活性逐渐升高(P<0.05);训练6周,仅有氧运动组升高(P<0.05),无氧运动组则活性降低(P<0.05).结果提示有氧训练更有利十保护大鼠骨骼肌肌浆网Na+,K+-ATP酶和Ca2+-ATP酶的活性,但需要一定的时间累积.     

白藜芦醇对离心运动后骨骼肌微损伤的修复

背景:白藜芦醇是一种天然的抗氧化剂和自由基廓清剂,具有清除自由基、减轻脂质过氧化等重要药理作用,目前有关白藜芦醇在减轻骨骼肌损伤、促进损伤修复方面的研究尚不多见.目的:观察白藜芦醇对离心运动后骨骼肌超微结构损伤、血清丙二醛和肌细胞浆Ca2+浓度的影响.设计、时间及地点:对照观察动物实验,于2007-08/2008-06在南方医科大学完成.材料:成年雄性SD大鼠72只,实验室适应性喂养3 d后随机分为蒸馏水组(n=40)、白藜芦醇组(n=32).白藜芦醇制剂购自湖南省洪江华光生物有限公司.方法:白藜芦醇组大鼠每日腹腔注射1次白藜芦醇制剂60mg/kg,蒸馏水组大鼠腹腔注射等量蒸馏水,连续2周.2周后,将大鼠在动物跑台上进行一次性下坡跑运动,速度为16 m/mjn,下坡坡度为16°,5 min运动,2 min休息,总运动时间为120 min.运动过程中采用人工驱赶和声刺激,不使用电刺激.主要观察指标:于运动前、运动后即刻、运动后24,48,72 h电镜下观察比目鱼肌纤维Z线,TAB法测定血清丙二醛和流式细胞仪检测肌细胞浆Ca2+浓度.结果:与蒸馏水组比较,白藜芦醇组镜下肌纤维损伤程度减轻,骨骼肌细胞Z线异常百分率在运动后即刻、运动后24,48,72 h比蒸馏水组分别降低了50.34%,52.67%,52.65%和53.26%(P＜0.05),离心运动引起的血清丙二醛升高程度分别下降了27.7%,29.56%,34.38%和27.79%(P＜0.05),胞浆Ca2+浓度分别降低了27.53%,25.84%,22.14%和11.62%(P＜0.05).结论:白藜芦醇可降低离心运动后血清丙二醛浓度和肌细胞浆Ca2+浓度,减轻运动导致的肌肉损伤.     

运动对1型糖尿病大鼠心肌肌浆网钙调控蛋白表达的影响

目的观察运动对1型糖尿病大鼠心肌肌浆网钙调控蛋白表达的影响，并探讨其机制。 方法选用健康Sprague-Dawley大鼠，随机分为正常对照组、运动对照组、糖尿病组和糖尿病+运动组，每组10只。用腹腔注射链脲佐菌素（55 mg/kg）法复制糖尿病模型，糖尿病+运动组大鼠在糖尿病模型建成后第4天开始跑台运动，于运动第4周末心脏采血，制备血清。采用放射免疫法测定血清胰岛素水平，采用RT-PCR法检测肌浆网Ca2+-ATP酶（SERCA）、磷酸受纳蛋白（PLB）和Ryanodine受体-2（RyR2）mRNA的表达，采用Western-blotting法检测SERCA2、PLB蛋白的表达。 结果与正常对照组相比，糖尿病组血糖、糖化血清蛋白及低密度脂蛋白水平升高，胰岛素和高密度脂蛋白水平降低，心肌SERCA2、PLB、RyR2 mRNA和SERCA2、PLB蛋白表达差异无统计学意义；糖尿病+运动组血糖水平升高，胰岛素水平降低，心肌SERCA2、PLB和RyR2的mRNA表达水平提高，SERCA2、PLB蛋白表达量增加，差异有统计学意义（P<0.01）。与糖尿病组相比，糖尿病+运动组大鼠糖化血清蛋白及低密度脂蛋白水平显著降低（P<0.01），SERCA2、PLB、RyR2 mRNA及SERCA2、PLB蛋白表达显著升高（P<0.01）。 结论运动对1型糖尿病大鼠心肌损伤有防治作用，其机制可能与运动上调SERCA2、PLB和RyR2的表达有关。     

运动对骨骼肌代谢的影响

受运动强度、运动量和运动状况等因素的影响,骨骼肌基本代谢发生变化,出现结构和功能上的适应：表现在骨骼肌细胞内的收缩成分、肌糖原、肌红蛋白增多,线粒体体积、数量增加,以及毛细胞 血管分布在骨骼肌上的密度加大等,使骨骼肌的有氧代谢能力加强,肌肉收缩效率提高,运动到力竭时间延长。同时指出急性运动时肌浆网结构改变和功能下降是诱发骨骼肌疲劳的重要原因,而高强度训练却可以提高肌浆网功能及Ca^2 摄取率,从而改善骨骼肌兴奋－收缩耦联的生理效能。并由此提出,抗阻力练习作为运动疗法的手段之一,可有效的增加肌肉力量和预防肌肉萎缩。     

运动对骨骼肌代谢的影响

受运动强度、运动量和运动状况等因素的影响,骨骼肌基本代谢发生变化,出现结构和功能上的适应表现在骨骼肌细胞内的收缩成分、肌糖原、肌红蛋白增多,线粒体体积、数量增加,以及毛细血管分布在骨骼肌上的密度加大等,使骨骼肌的有氧代谢能力加强,肌肉收缩效率提高,运动到力竭的时间延长。同时指出急性运动时肌浆网结构改变和功能下降是诱发骨骼肌疲劳的重要原因,而高强度训练却可以提高肌浆网功能及Ca     

急性缺氧时左室舒张功能障碍与心肌细胞肌浆网钙摄取功能的变化

临床上心室舒张功能障碍越来越引起人们的重视。为了研究急性缺氧左室舒张功能障碍时心肌细胞内肌浆网钙摄取功能，探讨左室舒张功能障碍发生的机理，该文用实验方法模拟临床上急性缺氧时左心室舒第功能障碍的情况（实验组），测定实验且和对照组民肌细胞浆风摄钙量和肌浆网钙ＡＴＰ酶活性。结果显示，实验组肌浆网摄钙量为５７．６±５．４ｎｍｏｌＣａ＾２＋／ｍｇＰｒ，对照组９６．１±７．２ｎｍｏｌＣａ＾２＋／ｍｇＰｒ，二者     

维生素E对离心运动大鼠骨骼肌超微结构的影响

背景:维生素E作为一种抗氧化剂,具有清除自由基的功效,可减轻运动中抗氧化酶所受的自由基损伤,减缓疲劳出现,从而提高运动能力.目的:通过维生素E对骨骼肌运动性损伤的干预,探讨其对骨骼肌运动性损伤形态学变化的影响,为骨骼肌运动性损伤的形态学研究和抗损伤机制的探索提供实验依据.设计、时间及地点:随机分组,动物实验,于2007-05/10在沈阳体育学院国家体育总局重点实验室和中国医科大学电镜中心完成.材料:雄性SD大鼠16只,随机均分为对照组、运动组、生理盐水组、维生素E组.方法:维牛索E组于实验前1 d腹腔注射维生素E胶丸,注射量为1.0-1.2mg/kg,总量为4mL/kg,每8 h注射1次,共4次.生理盐水组以生理盐水为对照,注射方式、注射量及处死时间同维生素E组.运动组只进行运动,不给予药物或生理盐水,对照组仅为常规饲养,无任何干预.采用一次力竭性下坡跑运动建造大鼠损伤模型,运动结束后,取大鼠右侧肱三头肌,制做电镜标本.主要观察指标:肌原纤维和肌节排列情况;Z线异常变化;细胞膜、细胞核、线粒体、肌浆网、T小管、卫星细胞等形态学改变.结果:补充维生素E组后,骨骼肌损伤的超微结构改变有明显的改善,虽然肌浆网尚有水肿表现,但肌纤维排列基本整齐,Z线明暗带清晰,细胞核清楚.结论:补充维牛素E可有效地减少离心运动对骨骼肌肌纤维损伤的形态学改变,肌纤维排列更加整齐、肌节更加清晰,其作用可能与维生素E的抗氧化和促进蛋白质的合成功能等因素有关.     

慢性心力衰竭犬心肌过表达肌浆网Ca~(2+)-ATP酶的安全性分析

目的研究心肌注射法转导肌浆网Ca2+-ATP酶(SERCA2a)基因治疗慢性心力衰竭犬的安全性。方法检测SER-CA2a基因转导心力衰竭犬的心肌酶学、心肌组织内cAMP含量、心肌耗氧量、心律失常及系统炎症指标、肝肾功能。结果 SER-CA2a基因转导治疗不增加细胞内cAMP浓度,心律失常的发生率和心肌氧耗未增加,未引起明显的全身炎症反应和肝肾功能的损伤。结论 SERCA2a基因转导是一种安全的治疗策略。     

热应激预处理对离心运动大鼠骨骼肌自由基代谢的影响

背景：研究表明热预处理能够提高肌肉抗损伤的能力,但具体的机制尚不清楚。目的：观察热应激预处理对离心运动大鼠骨骼肌超氧化物歧化酶活性及丙二醛含量的影响。方法：雄性Wistar大鼠随机分为对照组、离心运动组、预热应激＋离心运动组。热应激温度为43℃,时间约35min。采用-16°下坡跑台跑做大负荷间歇性离心运动,跑速为26.8m/min,运动5min,间歇1min,共进行10组。分别于运动前1h、运动后1,24,48h取大鼠腓肠肌,采用硫代巴比妥酸法测定大鼠丙二醛含量,黄嘌呤氧化酶法测定超氧化物歧化酶活性。结果与结论：与对照组比较,离心运动组大鼠腓肠肌丙二醛含量显著增高（P〈0.05）,并随运动后时间的延长逐渐升高,超氧化物歧化酶活性随运动后时间的延长显著降低（P〈0.05）。与离心运动组比较,预热应激＋离心运动组大鼠腓肠肌超氧化物歧化酶活性显著增高（P〈0.05）,丙二醛含量显著降低（P〈0.05）。说明热应激预处理可增强骨骼肌超氧化物歧化酶活性,降低丙二醛含量,对离心运动损伤有保护作用。     

Muscle oxygenation after downhill walking-induced muscle damage

The purpose of this study was to investigate changes in muscle oxygenation and blood flow within vastus lateralis after an exhaustive session of downhill walking (DW). Nine healthy males performed 40-min DW on a treadmill with a gradient of -25% and at walking velocity of 6.4 km h(-1). To increase the likelihood that DW would induce muscle damage, subjects were loaded with 5% of their body weight carried in a back pack. Before and after DW exercise on day 1 and over the next 4 days, maximum voluntary contractions (MVCs), subjects' perception of muscle soreness (SOR), plasma creatine kinase (CK) activity and myoglobin (Mb) concentrations, and muscle oxygenation (using near infrared spectroscopy; NIRS) within vastus lateralis were assessed. Repeated-measures anova revealed that MVC decreased while SOR and Mb concentration increase significantly (P<0.05) after DW, consistent with its effectiveness to evoke muscle damage. Resting tissue oxygen saturation increased immediately after DW, but recovered within 24 h. During isometric contractions at 30%, 50% and 80% of MVC, oxygen desaturation and re-saturation kinetics became significantly faster than pre-exercise values. The possible mechanism responsible for these changes might be increased resting muscle oxygen utilization after muscle damage because of an increased requirement for aerobic energy-demanding repair processes.     

Calcium transport by skeletal muscle sarcoplasmic reticulum in the hypothyroid rat

The rate of calcium transport by isolated sarcoplasmic reticulum from rat skeletal muscle increases markedly during the first 4 wk of life and thereafter remains relatively constant. When animals are made hypothyroid during the first 3 wk of life, there is a marked inhibition of the increase in calcium transport by the sarcoplasmic reticulum. Production of hypothyroidism after 4 wk of age, at which time the calcium transport by sarcoplasmic reticulum has reached maximum levels, results in a depression in the rate of calcium transport. There is no clear alteration in ATPase activity of the sarcoplasmic reticulum to account for the low calcium transport in hypothyroidism. It is proposed that the decrease in calcium transport by sarcoplasmic reticulum may account for observed alterations in the intrinsic contractile properties of muscle in the hypothyroid animal.     

Calcium transport by skeletal muscle sarcoplasmic reticulum in the hypothyroid rat

The rate of calcium transport by isolated sarcoplasmic reticulum from rat skeletal muscle increases markedly during the first 4 wk of life and thereafter remains relatively constant. When animals are made hypothyroid during the first 3 wk of life, there is a marked inhibition of the increase in calcium transport by the sarcoplasmic reticulum. Production of hypothyroidism after 4 wk of age, at which time the calcium transport by sarcoplasmic reticulum has reached maximum levels, results in a depression in the rate of calcium transport. There is no clear alteration in ATPase activity of the sarcoplasmic reticulum to account for the low calcium transport in hypothyroidism. It is proposed that the decrease in calcium transport by sarcoplasmic reticulum may account for observed alterations in the intrinsic contractile properties of muscle in the hypothyroid animal.     

Effect of vitamin D deficiency on sarcoplasmic reticulum function and troponin C concentration of rabbit skeletal muscle.

1. Weanling rabbits were made rachitic either by a vitamin D-deficient diet or by parenteral administration of ethane 1-hydroxy-1,1-diphosphonate (EHDP) in amounts sufficient in other species to block the formation of 1,25-dihydroxycholecalciferol [1,25-(OH)2D3]. 2. The uptake of calcium into the isolated sarcoplasmic reticulum from mixed striated quadriceps muscle, and the amount of troponin C (the calcium-binding component of the troponin complex) in relation to other proteins from the same muscle, were measured. 3. In muscle from animals made rachitic by a dietary deficiency of vitamin D, the rate of uptake of calcium by the sarcoplasmic reticulum and the troponin C concentration were both significantly less (P less than 0.02) than in control littermates. In EHDP-treated animals no significant differences from controls were found. 4. These results show that dietary deficiency of vitamin D in such animals can affect muscle physiology. Since no changes are found in animals made rachitic with EHDP, who presumably have a selective deficiency of 1,25-(OH)2D3, it is possible that the effect of vitamin D on muscle is mediated through metabolites other than 1,25-(OH)2D3 such as 25-hydroxycholecalciferol.     

耐力训练后减量训练模型大鼠骨骼肌肌浆网Ca2+的转运功能

背景:运动训练对骨骼肌超微结构的影响是运动医学中定量化的细胞生物学研究热点.目的:观察大鼠耐力训练后减量训练模型骨骼肌肌浆网的钙离子转运功能的变化.设计、时间及地点:随机对照动物实验,动物训练于2006-04/07在西安体育学院进行,生化实验于2006-07在西安交通大学生物实验中心完成.材料:2月龄雄性健康SD大鼠39只,体质量(220±20)g.方法:5只SD大鼠用于预实验.其余大鼠随机分为正常对照组8只、耐力训练组8只、耐力减训组18只.耐力训练组和耐力减训组递增训练周期均为6周,6周后将耐力减训组根据减训周期随机分为耐力减训2周,4周,6周组.对训练大鼠采用小动物跑台进行递增耐力负荷训练,减训组采用逐渐减少运动强度训练.主要观察指标:使片j酶偶联法测定大鼠腓肠肌肌浆网Ca2 -ATPase的活性;采用荧光分光光度计测量肌浆网最大Ca2 摄取量和释放量.结果:①肌浆网SRCa2 -ATP ase活性:耐力训练组较正常对照组显著性增加(P<0.01);耐力减训2周组与耐力训练组比较基本不变(P>0.05):耐力减训4周,6周组较耐力训练组下降(P<0.01).②肌浆网SR最大Ca2 摄取和释放率:耐力训练组显著性增加(P<0.01);耐力减训2周组与耐力训练组比较差异无显著性意义(P>0.05);耐力减训4周,6周组下降显著(P<0.01).结论:耐力训练6周后,SD大鼠骨骼肌肌浆网Ca2 ATPase的活性增强,钙离子的摄取和释放率增加.减量训练2周骨骼肌肌浆网Ca2 ATPase的活性、钙离子摄取和释放率下降不明显.4周更长时间骨骼肌肌浆网Ca2 ATPase的活性及钙离子摄取和释放率下降明显.     

外源性磷酸肌酸对游泳力竭小鼠大脑中谷氨酸和钙-ATP酶活力的影响

目的：研究外源性磷酸肌酸（PCr）对游泳力竭小鼠大脑中谷氨酸（Glu）和钙-ATP酶（Ca^2＋ATPase）活力的影响,以进一步揭示PCr的抗疲劳机制。方法：将44只6周龄小鼠分为力竭对照组12只（A组）、力竭给药组12只（B组）、游泳8min对照组10只（C组）、游泳8min给药组10只（D组）,采取小鼠负重游泳的力竭运动模型,每只小鼠负重量为自身体质量的6％。于游泳前30min,B、D组小鼠经腹腔注射磷酸肌酸钠溶液1000mg／kg;A、C组小鼠注射同等比例生理盐水作为安慰剂。记录力竭组小鼠的力竭游泳时间,采用化学比色法检测4组小鼠大脑中Glu含量和Ca^2＋ATPase的活性。结果：经检测,B组小鼠的力竭游泳时间明显长于A组（P〈0．05）。小鼠大脑Glu含量检测显示,B组明显低于A组,D组明显低于c组（P％0．05）;Ca^2＋ATPase活力检测显示,B组明显高于A组,D组明显高于C组（P〈0．05）。结论：外源性PCr的抗疲劳机制与增强Ca^2＋ATPase活性和间接降低大脑中的Glu含量有关。     

急性离心运动后恢复期大鼠骨骼肌微管形态及自噬体降解特征研究

目的:观察急性离心运动后恢复期大鼠骨骼肌微管形态变化及自噬体降解特征.方法:SD大鼠随机分为安静组、急性离心运动组,于运动后0h、12h、24h、48h、72h取材.分离单根肌纤维检测微管形态,Western Blot检测LC3、p62蛋白表达,腹腔注射秋水仙碱检测恢复前期(12h内)骨骼肌自噬流.结果:①急性离心运动...     

Effect of resistance exercise on insulin sensitivity of skeletal muscle

Insulin resistance (IR) is the common pathophysiological basis of many metabolic diseases. IR is characterized by decreased glucose uptake in skeletal muscle and adipose tissue, especially in skeletal muscle. Skeletal muscle is the main target tissue of glucose uptake under insulin stimulation. Glucose uptake by skeletal muscle is complex, and it is controlled by many pathways. The PI3K/AKt/GSK-1 signaling pathway is not only the main pathway for insulin signal transduction but also an important mechanism for regulating blood glucose. From the binding of insulin to its receptors on the surface of target cells to the transportation of glucose from extracellular fluid to skeletal muscle, a series of signal transduction processes is completed, any of which potentially affects the physiological effects of insulin and leads to IR. Resistance exercise (RT) can reduce skeletal muscle IR and effectively improve blood glucose control and glycosylated hemoglobin level in patients with type 2 diabetes mellitus (T2DM). However, the exact mechanism by which RT improves skeletal muscle IR remains unclear. Therefore, this paper discusses the above problems by tracking the progress of the literature to deepen the correlation between RT and skeletal muscle insulin sensitivity and provide further evidence for the application of exercise therapy in IR. In conclusion, RT mainly improves insulin sensitivity of skeletal muscle by increasing muscle mass, microvascular blood flow, and glucose transporter-4 expression in skeletal muscle, as well as by reducing lipid accumulation and inflammation in skeletal muscle. Thus, it is potentially useful in the prevention and treatment of T2DM.     

离心跑台运动对小鼠骨骼肌炎性因子、肌再生因子及血管再生因子表达的影响

目的:观察小鼠离心运动后骨骼肌炎性因子、肌再生因子以及血管再生因子的表达变化,探讨其在离心运动骨骼肌损伤修复中可能发挥的作用。方法:32只雄性C57BL/6小鼠随机分为对照组(C组,n=8)和离心运动组(D组,n=24)。根据取材时间,离心运动组又分为3个小组(运动后1d,3d和7d组)。离心运动后不同时间点取双侧腓肠肌。HE染色观察骨骼肌形态学变化,比色法检测血浆肌酸激酶(CK)和乳酸脱氢酶(LDH)活性,荧光定量PCR检测炎性因子、肌再生因子及血管再生因子基因表达的变化。结果:小鼠下坡跑后骨骼肌纤维结构无明显破坏,无显著炎性细胞浸润。与对照相比,血浆CK和LDH活性在运动后各时间点均无显著变化(P0.05)。从基因层面看,炎性细胞标志物(MPO—嗜中性粒细胞标志物;F4/80—巨噬细胞标志物)在下坡跑后显著上升。部分炎症因子(如肿瘤坏死因子-α、白介素-1β、白介素-6)在下坡跑后显著上调。而肌再生调节因子中,只有机械生长因子和白血病抑制因子在运动后出现显著上调。而肌再生关键细胞——肌卫星细胞的特异性标记分子(分子标志—Pax7,增殖标记—Myo D,分化标记—myogenin)在离心运动后未出现显著变化(P0.05)。此外,其他与肌肉和血管再生密切相关的再生因子(如:胰岛素样生长因子1、肝细胞生长因子、尿激酶型纤溶酶原激活物、环氧合酶2、低氧诱导因子-1α、血管内皮生长因子、血管生成素1等)在离心运动后均未见显著变化(P0.05)。结论:从形态学表现、血清指标和基因表达综合来看,离心跑台运动并非小鼠骨骼肌损伤建模的理想方式。     

游泳运动对大鼠心房肌细胞超微结构的影响

目的:探讨不同运动量游泳运动对大鼠心房肌细胞超微结构的影响,以期为运动对心肌的生理和病理变化研究提供参考资料.方法:SD大鼠分为不同运动量运动组和力竭运动组,前者进行12周的低、中和高运动量游泳运动,后者进行1次力竭游泳运动.取右心房肌组织进行常规透射电镜样品制备,透射电镜观察心房肌细胞超微结构的变化.结果:低和中运动量运动可使肌原纤维排列整齐,Z线变粗,Ⅰ带增宽;线粒体数量增加,嵴密集排列;内质网和高尔基体丰富,合成大量心钠肽,并快速地分泌到细胞外;细胞连接增强.高运动量运动,导致肌原纤维部分Z线紊乱,核膜内陷,线粒体嵴疏松,细胞连接减弱.力竭运动对肌原纤维损伤较重,细胞核染色质固缩凝集,线粒体形态改变,嵴消失;但肌原纤维和线粒体的形态结构在力竭后24h得以部分恢复.结论:高运动量和力竭运动可以导致心房肌超微结构破坏.