牛磺酸对运动大鼠心肌线粒体游离钙、PLA2及脂质过氧化的影响

目的 探讨牛磺酸对运动大鼠心肌线粒体损伤的保护作用.方法 以大鼠力竭运动为模型,观察了牛磺酸对运动后大鼠心肌线粒体脂质过氧化水平、抗氧化酶、游离钙及磷脂酶A2（PLA2）的影响.结果 力竭运动可引起大鼠心肌线粒体脂质过氧化水平和磷脂酶A,活性显著升高,心肌线粒体超氧化物歧化酶（SOD）活性和游离钙浓度的显著下降,而牛磺酸可抑制人鼠力竭运动后心肌线粒体脂质过氧化水平和磷脂酶A：活性的显著升高,抑制大鼠心肌线粒体SOD的活性和游离钙浓度的显著下降.结论 牛磺酸可减少力竭运动后自由基对心肌线粒体的攻击,具有保护力竭运动后心肌线粒体的功能和防止心肌损伤的作用.     

牛磺酸对运动大鼠心肌线粒体游离钙、PLA2及脂质过氧化的影响

目的：探讨牛磺酸对运动大鼠心肌线粒体损伤的保护作用，方法：以大鼠力竭运动为模型，观察了牛磺酸对运动后大鼠心肌线粒体脂质过氧化水平，抗氧化酶，游离钙及磷脂酶A2（PLA2）的影响。结果：力竭运动可引起大鼠心肌线粒体脂质过氧化水平和PLA2活性显著升高，心肌线粒体超氧化物歧化酶（SOD）活性和游离钙浓度的显著下降，而牛磺酸可抑制大鼠力竭运动后心肌线粒体脂质过氧化水平和PLA2活性的显著升高，抑制大鼠心肌线粒体SOD的活性和游离钙浓度的显著下降，结论：牛磺酸可减少力竭运动后自由基对心肌线粒体的攻击，具有保护力竭运动后心肌线粒体的功能和防止心肌损伤的作用。     

不同强度运动对大鼠心肌线粒体功能的影响

目的 探讨不同强度运动对心肌线粒体功能的影响及与运动性疲劳的关系。方法 以不同时间游泳为运动模式，观察了９０ｍｉｎ运动、力竭运动和力竭运动后２４ｈ心肌线粒体脂质过氧化水平、抗抗化能力、游离钙浓度及磷脂酶Ａ２活性的变化。结果 ９０ｍｉｎ运动后心肌线粒全和项指标未见明显变化。力竭运动后心肌线粒体脂质过氧化水平显提高，抗经能力和游离肌损伤，适度运动不造成线粒体和心肌损伤。     

急性运动对小鼠心肌线粒体功能的影响

目的：探讨不同强度运动对心肌线粒体功能的影响。方法：40只小鼠随机分为安静对照组（A组）、90min运动组（B组）、力竭组（C组）及力竭后恢复24h组（D组）各10只，以游泳为运动方式，观察各组血清肌酸激酶（CK）、乳酸脱氢酶（LDH）、ATP合成活性及脂质过氧化水平丙二醛（MDA）的变化，并在光镜和电镜下观察心肌超微结构。结果：与A组比较，C组血清CK、LDH水平及心肌MDA水平显著增高（P〈0．05）．ATP合成能力显著下降（P〈0．05），电镜下心肌超微结构损伤明显。结论：急性力竭运动可造成线粒体损伤和心肌损伤，力竭运动后24h各项指标基本恢复。     

牛磺酸对力竭运动大鼠白肌线粒体的保护作用

目的探讨外源性牛磺酸对力竭运动后大鼠白肌线粒体自由基代谢的影响,从亚细胞水平研究牛磺酸抗运动性疲劳的机制。方法以大鼠力竭性运动为模型,观察了牛磺酸对力竭运动时大鼠白肌线粒体脂质过氧化、抗氧化系统及总Ca2+浓度的影响。结果牛磺酸可降低大鼠力竭运动后白肌线粒体脂质过氧化水平,提高大鼠力竭运动后白肌线粒体超氧化物歧化酶(SOD)的活性,保持大鼠力竭运动后白肌线粒体还原性谷胱甘肽含量及总Ca2+浓度。结论牛磺酸可减少力竭运动后因脂质过氧化而产生的自由基,降低自由基对白肌线粒体的攻击,维持线粒体膜的功能。     

牛磺酸对力竭运动大鼠白肌线粒体的保护作用

目的 探讨外源性牛磺酸对力竭运动后大鼠白肌线粒体自由基代谢的影响，从亚细胞水平研究牛磺酸抗运动性疲劳的机制。方法 以大鼠力竭性运动为模型，观察了牛磺酸对力竭运动时大鼠白肌线粒体脂质过氧化、抗氧化系统及总Ca^2 浓度的影响。结果 牛磺酸可降低大鼠力竭运动后白肌线粒体脂质过氧化水平，提高大鼠力竭运动后白肌线粒体超氧化物歧化酶(SOD)的活性，保持大鼠力竭运动后白肌线粒体还原性谷胱甘肽含量及总Ca^2 浓度。结论 牛磺酸可减少力竭运动后因脂质过氧化而产生的自由基，降低自由基对白肌线粒体的攻击，维持线粒体膜的功能。     

螺旋藻对力竭运动大鼠心肌损伤的保护作用

目的:观察螺旋藻对力竭运动大鼠心肌线粒体丙二醛、钙离子浓度及超氧化物歧化酶、磷脂酶A2活性的影响。方法:实验于2002-09/2003-03在广西医科大学生理实验室完成。选择成年SD雄性大鼠30只,随机分为安静组、力竭运动组、螺旋藻力竭运动组,每组10只。安静组、力竭运动组喂普通饲料,螺旋藻力竭运动组在饲料中加入15%螺旋藻干粉喂养,共喂养4周。力竭运动组、螺旋藻力竭运动组大鼠在跑台上进行下坡运动至力竭,跑台速度16m/min,坡度为-16°,力竭标准为动物已跟不上预定速度,经电刺激尾巴仍不能继续往前跑。力竭运动组、螺旋藻力竭运动组大鼠力竭后即刻断头处死,同时亦将安静组处死,迅速取心室肌组织,观察各组大鼠心肌线粒体丙二醛、钙离子浓度、磷脂酶A2和超氧化物歧化酶的活性。结果:30只大鼠全部进入结果分析。①大鼠心肌线粒体丙二醛、钙离子浓度和磷脂酶A2活性:力竭运动组显著高于安静组[(21.12±2.66)μmol/g,(13.68±2.90)μmol/g;(31.66±4.83)μmol/g,(16.83±4.45)μmol/g;(1792.44±145.48)μkat/g,(604.09±53.04)μkat/g,q=16.97,10.54,39.21,P<0.01],螺旋藻力竭运动组[(17.40±1.38)μmol/g,(20.74±4.01)μmol/g,(1040.75±59.81)μkat/g]显著低于力竭运动组(q=4.51,7.76,24.80,P<0.01)。②心肌线粒体超氧化物歧化酶活性:力竭运动组明显低于安静组[(306.09±24.44)μkat/g,(474.29±27.50)μkat/g,q=22.86,P<0.01]。螺旋藻力竭运动组[(372.60±19.61)μkat/g]明显高于力竭运动组(q=22.86,P<0.01)。结论:力竭运动引起心肌线粒体丙二醛、钙离子浓度及磷脂酶A2活性的升高,超氧化物歧化酶活性下降,造成心肌线粒体和心肌的损伤;螺旋藻可抑制力竭运动后心肌线粒体的上述变化而起到保护心肌,抗运动性损伤的作用。     

中药养阴活血方对力竭运动小鼠组织超微结构及自由基代谢的影响

目的:探讨中药养阴活血方对运动应激损伤的防治作用。方法:实验于1999-09/2000-01在南京医科大学动物实验中心完成。选用30只昆明种雄性小鼠,随机分为3组,每组10只。对照组:静脉注射生理盐水0.3mL/d。造型组:静脉注射生理盐水0.3mL/d30min后游泳。药物造型组:静脉注射药物注射液0.3mL/d30min后游泳。除对照组外其余两组均建立负重力竭游泳运动模型,观察养阴活血注射液对力竭运动小鼠心肌、骨骼肌、肝脏细胞超微结构及组织中超氧化物歧化酶、过氧化脂质、谷胱甘肽过氧化物酶的影响。结果:30只大鼠均进入结果分析,无脱失值。①各组小鼠肝、心肌、骨骼肌超氧化物歧化酶活性、谷胱甘肽过氧化物酶活性、过氧化脂质含量的比较:力竭运动后造型组肝脏超氧化物歧化酶活性显著下降,心肌超氧化物歧化酶活性呈升高趋势。药物造型组组织超氧化物歧化酶活性均有升高,其中心肌、骨骼肌增高差异显著;力竭运动后造型组肝脏谷胱甘肽过氧化物酶活性显著下降,心肌谷胱甘肽过氧化物酶活性则呈显著升高。药物造型组的组织谷胱甘肽过氧化物酶活性均有升高,其中心肌、肝脏谷胱甘肽过氧化物酶活性增高差异显著;力竭运动后造型组肝、心肌、骨骼肌过氧化脂质含量均有显著升高。应用中药养阴活血方使组织过氧化脂质含量均有降低,其中肝脏、骨骼肌降低差异显著。②各组小鼠肝、心肌、骨骼肌组织超微结构的比较:对照组小鼠肝、心肌、骨骼肌呈正常超微结构形态;造型组细胞胞质呈无定形大小不等空泡,内质网及糖原基本消失,线粒体隐约可见,心肌肌原纤维排列有紊乱现象,骨骼肌肌原纤维疏松变细;药物造型组肝细胞内质网及线粒体均清晰可见,细胞核呈正常结构。结论:力竭运动使小鼠肝脏、心肌、骨骼肌细胞超微结构显著受损,过氧化脂质含量升高、超氧化物歧化酶、谷胱甘肽过氧化物酶活性紊乱。养阴活血方具有激发内源性抗氧化酶活性、抗脂质过氧化、缓解力竭运动所致组织损伤作用。     

螺旋藻对力竭运动大鼠心肌损伤的保护作用

目的：观察螺旋藻对力竭运动大鼠心肌线粒体丙二醛、钙离子浓度及超氧化物歧化酶、磷脂酶A2活性的影响。方法：实验于2002-09／2003-03在广西医科大学生理实验室完成。选择成年SD雄性大鼠30只，随机分为安静组、力竭运动组、螺旋藻力竭运动组，每组10只。安静组、力竭运动组喂普通饲料，螺旋藻力竭运动组在饲料中加入15％螺旋藻干粉喂养，共喂养4周。力竭运动组、螺旋藻力竭运动组大鼠在跑台上进行下坡运动至力竭，跑台速度16m／min，坡度为-16&;#176;，力竭标准为动物已跟不上预定速度，经电刺激尾巴仍不能继续往前跑。力竭运动组、螺旋藻力竭运动组大鼠力竭后即刻断头处死，同时亦将安静组处死，迅速取心室肌组织，观察各组大鼠心肌线粒体丙二醛、钙离子浓度、磷脂酶A：和超氧化物歧化酶的活性。结果：30只大鼠全部进入结果分析。①大鼠心肌线粒体丙二醛、钙离子浓度和磷脂酶A2活性：力竭运动组显著高于安静组[(21．12&;#177;2．66)μmol／g，(13．68&;#177;2．90)μmol／g；(31．66&;#177;4．83)μmol／g(16．83&;#177;4．45)μmol／g；(1792．44&;#177;145.48)μkat／g，(604．09&;#177;53．04)μkat／g，q=16．97，10．54，39．21，P&;lt;0．01]，螺旋藻力竭运动组[(17．40&;#177;1．38)μmol／g，(20．74&;#177;4．01)μmol／g，(1040.75&;#177;59．81)μkat／g]显著低于力竭运动组(q=451，7．76，24.80，P&;lt;0．01)。②心肌线粒体超氧化物歧化酶活性：力竭运动组明显低于安静组[(306．09&;#177;9444)μkat／g／g，(474．29&;#177;．2750)μkat／g，q=22.86,P&;lt;0．01]。螺旋藻力竭运动组[(372．60&;#177;19．61)μkat／g明显高于力竭运动组(q=22．86,P&;lt;0．01)。结论：力竭运动引起心肌线粒体丙二醛、钙离子浓度及磷脂酶A2活性的升高，超氧化物歧化酶活性下降，造成心肌线粒体和心肌的损伤；螺旋藻可抑制力竭运动后心肌线粒体的上述变化而起到保护心肌，抗运动性损伤的作用。     

中药养阴活血方对力竭运动小鼠组织超微结构及自由基代谢的影响

目的：探讨中药养阴活血方对运动应激损伤的防治作用.方法：实验于1999-09/2000-01在南京医科大学动物实验中心完成.选用30只昆明种雄性小鼠,随机分为3组,每组10只.对照组：静脉注射生理盐水0.3 mL/d.造型组：静脉注射生理盐水0.3 mL/d 30 min后游泳.药物造型组：静脉注射药物注射液0.3 mL/d 30 min后游泳.除对照组外其余两组均建立负重力竭游泳运动模型,观察养阴活血注射液对力竭运动小鼠心肌、骨骼肌、肝脏细胞超微结构及组织中超氧化物歧化酶、过氧化脂质、谷胱甘肽过氧化物酶的影响.结果：30只大鼠均进入结果分析,无脱失值.①各组小鼠肝、心肌、骨骼肌超氧化物歧化酶活性、谷胱甘肽过氧化物酶活性、过氧化脂质含量的比较：力竭运动后造型组肝脏超氧化物歧化酶活性显著下降,心肌超氧化物歧化酶活性呈升高趋势.药物造型组组织超氧化物歧化酶活性均有升高,其中心肌、骨骼肌增高差异显著;力竭运动后造型组肝脏谷胱甘肽过氧化物酶活性显著下降,心肌谷胱甘肽过氧化物酶活性则呈显著升高.药物造型组的组织谷胱甘肽过氧化物酶活性均有升高,其中心肌、肝脏谷胱甘肽过氧化物酶活性增高差异显著;力竭运动后造型组肝、心肌、骨骼肌过氧化脂质含量均有显著升高.应用中药养阴活血方使组织过氧化脂质含量均有降低,其中肝脏、骨骼肌降低差异显著.②各组小鼠肝、心肌、骨骼肌组织超微结构的比较：对照组小鼠肝、心肌、骨骼肌呈正常超微结构形态;造型组细胞胞质呈无定形大小不等空泡,内质网及糖原基本消失,线粒体隐约可见,心肌肌原纤维排列有紊乱现象,骨骼肌肌原纤维疏松变细;药物造型组肝细胞内质网及线粒体均清晰可见,细胞核呈正常结构.结论：力竭运动使小鼠肝脏、心肌、骨骼肌细胞超微结构显著受损,过氧化脂质含量升高、超氧化物歧化酶、谷胱甘肽过氧化物酶活性紊乱.养阴活血方具有激发内源性抗氧化酶活性、抗脂质过氧化、缓解力竭运动所致组织损伤作用.     

牛磺酸对运动大鼠心肌线粒体ATP酶及钙、镁离子的影响

目的：探讨牛磺酸对运动大鼠心肌线粒体ATP酶及钙、镁离子的影响。方法：以力竭运动大鼠为模型，测定了心肌线粒体Ca^2 -ATP酶、Mg^2 -ATP酶的活性以及Ca^2 、Mg^2 含量。结果：大鼠力竭运动后，心肌线粒体Ca^2 -ATP酶和Mg^2 -ATP酶的活性显著下降，Ca^2 -含量显著增加，Mg^2 含量显著降低；而补充牛磺酸组大鼠力竭运动后未见心肌线粒体Ca^2 -ATP酶和Mg^2 -ATP酶的活性以及Ca^2 -、Mg^2 含量的显著变化。结论：牛磺酸能有效地拮抗力竭运动后大鼠心肌线粒体Ca^2 -ATP酶、Mg^2 -ATP酶活性的降低以及Ca^2 -、Mg^2 含量的显著变化，具有保护心肌线粒体的作用。     

Exhaustive exercise increases plasma/serum total oxidation resistance in moderately trained men and women,whereas their VLDL + LDL lipoprotein fraction is more susceptible to oxidation

The purpose of this study was to evaluate the effects of exhaustive exercise (marathon run) on different lipid peroxidation measurements, including copper-induced serum lipids and VLDL + LDL oxidation susceptibility, and on plasma total antioxidative capacity (TRAP), muscular damage and plasma antioxidants in healthy moderately trained male (n = 21) and female (n = 25) volunteers. Blood samples were taken before and just after the 42-km run. In women, baseline levels of several antioxidative compounds (serum albumin and uric acid, plasma free thiols and blood glutathione) were lower, resulting in 21.5% lower plasma total antioxidative capacity and 70.3% higher serum oxidation susceptibility, compared to men. To compare effects in men and women, the exercise-induced variable changes were adjusted for their baseline levels. After this adjustment, there were no statistically significant differences between the genders in the extent of muscular damage (serum creatine kinase, (CK)), or in the change in serum lipids or VLDL + LDL oxidation susceptibility, or that of plasma antioxidative capacity. A possible beneficial effect of exercise was that serum HDL cholesterol levels increased significantly in both genders, but especially in women. In the group of pooled genders (n=46), the increases in serum CK and in plasma lactate were 190% (95% CI, 133% to 246%) and 109% (95% CI, 65% to 175%), respectively. On the basis of our lipid peroxidation and TRAP measurements, uric acid was observed to be the most important plasma antioxidant. The effect of exercise was to decrease the oxidation susceptibility of serum lipids by 24.8% (95% CI 13.4% to 36.2%) and to elevate plasma TRAP by 14.6% (95% CI, 11.4% to 17.7%). Nonetheless, the oxidation susceptibility of the VLDL + LDL fraction increased by 11.0% (95% CI, 1.9% to 20.2%). Our results suggest that there are no gender-based differences in exhaustive exercise-induced lipid peroxidation or muscular damage. Secondly, even though exhaustive exercise can increase plasma/serum total resistance towards oxidation, the oxidation resistance of the atherogenic lipoprotein fraction might be diminished. On the basis of these results, several in vitro measurements of lipid peroxidation assessing both water and lipid soluble plasma fractions are needed if a true perspective of the plasma redox status is to be obtained.     

Effects of copper deficiency on carbon tetrachloride-induced lipid peroxidation

To investigate the hypothesis that copper deficiency in the rat could result in increased susceptibility to CCl4-induced lipid peroxidation caused by decreased free radical defenses, we performed a series of experiments administering CCl4 to copper-deficient and control rats. Peroxidation after CCl4 administration was monitored by measuring the evolution of expired ethane in closed metabolic chambers. Rats were fed one of two copper-deficient diets based on either evaporated milk or powdered milk. Compared with control values, liver copper content, liver superoxide dismutase activity, and plasma ceruloplasmin level were significantly decreased in copper-deficient rats fed either of the diets. Liver glutathione peroxidase activity was also decreased in the copper-deficient rats fed the evaporated milk diet. Ethane evolution was markedly increased in both copper-deficient groups as compared with their controls. Copper deficiency was also found to produce increases in hepatic iron concentrations, but normal rats loaded with iron dextran to increase hepatic iron concentrations into a range similar to that found in the copper-deficient rats did not exhibit increased ethane evolution after CCl4 administration. Copper deficiency in the rat results in increased CCl4-induced lipid peroxidation.     

Exhaustive exercise increases plasma/serum total oxidation resistance in moderately trained men and women,whereas their VLDL+ LDL lipoprotein fraction is more susceptible to oxidation

The purpose of this study was to evaluate the effects of exhaustive exercise (marathon run) on different lipid peroxidation measurements, including copper-induced serum lipids and VLDL+ LDL oxidation susceptibility, and on plasma total antioxidative capacity (TRAP), muscular damage and plasma antioxidants in healthy moderately trained male (n= 21) and female (n= 25) volunteers. Blood samples were taken before and just after the 42-km run. In women, baseline levels of several antioxidative compounds (serum albumin and uric acid, plasma free thiols and blood glutathione) were lower, resulting in 21.5% lower plasma total antioxidative capacity and 70.3% higher serum oxidation susceptibility, compared to men. To compare effects in men and women, the exercise-induced variable changes were adjusted for their baseline levels. After this adjustment, there were no statistically significant differences between the genders in the extent of muscular damage (serum creatine kinase, (CK)), or in the change in serum lipids or VLDL+ LDL oxidation susceptibility, or that of plasma antioxidative capacity. A possible beneficial effect of exercise was that serum HDL cholesterol levels increased significantly in both genders, but especially in women. In the group of pooled genders (n= 46), the increases in serum CK and in plasma lactate were 190% (95% CI, 133% to 246%) and 109% (95% CI, 65% to 175%), respectively. On the basis of our lipid peroxidation and TRAP measurements, uric acid was observed to be the most important plasma antioxidant. The effect of exercise was to decrease the oxidation susceptibility of serum lipids by 24.8% (95% CI 13.4% to 36.2%) and to elevate plasma TRAP by 14.6% (95% CI, 11.4% to 17.7%). Nonetheless, the oxidation susceptibility of the VLDL+ LDL fraction increased by 11.0% (95% CI, 1.9% to 20.2%). Our results suggest that there are no gender-based differences in exhaustive exercise-induced lipid peroxidation or muscular damage. Secondly, even though exhaustive exercise can increase plasma/serum total resistance towards oxidation, the oxidation resistance of the atherogenic lipoprotein fraction might be diminished. On the basis of these results, several in vitro measurements of lipid peroxidation assessing both water and lipid soluble plasma fractions are needed if a true perspective of the plasma redox status is to be obtained.     

Hepatic injury and lipid peroxidation during ischemia and reperfusion

We determined the relationship between lipid peroxidation and alterations in hepatic secretory and microsomal function during various periods of hepatic ischemia/reperfusion. Rats were pretreated with alpha-tocopherol or vehicle and then subjected to 30, 60, and 90 min, no-flow hepatic ischemia in vivo with 1 or 5 h of reperfusion. Serum aminotransferase (ALT) level, wet-dry weight ratio, and lipid peroxidation were increased at 1 and 5 h of reperfusion, and these changes were significantly attenuated by alpha-tocopherol. Na+, K+-ATPase activity, and glucose-6-phosphatase activity were significantly decreased in 90-min ischemic rats, and these decreases were ameliorated by alpha-tocopherol. After 90 min of ischemia, bile flow, cholate output, and bilirubin output were markedly decreased by ischemia/reperfusion, and alpha-tocopherol restored the secretion. Cytochrome P450 content was decreased by ischemia/reperfusion and restored by alpha-tocopherol to the level of that found in the sham-operated group. Aminopyrine N-demethylase activity was decreased, and aniline p-hydroxylase was increased in 60-min ischemic rats. The changes in the activities of the two enzymes were prevented by alpha-tocopherol. Our findings suggest that ischemia/reperfusion diminishes hepatic secretory functions and microsomal drug metabolizing systems in proportion to the duration of ischemia and reperfusion in vivo, and this is associated with increased lipid peroxidation.     

大鼠内毒素血症早期肝细胞线粒体的氧化损伤及中药912液的干预作用

目的：通过动物实验观察内毒血症早期大鼠肝细胞线粒体的氧化损伤及中药912液的保护作用。方法：将大鼠随机分为空白对照组、内毒素组、内毒素＋912液组、内毒素＋盐水对照组。提取内毒素血症大鼠肝细胞粒体测定其超氧阴离子生成量,同时测定线粒体及血清中GSH－Px,SOD,并观察中药912液的作用。结果：内霉素血症大鼠肝细胞线粒体超氧阴离子生成量及MDA明显升高;血清中MDA增多,而SOD减少。912液治疗后内毒素血症大鼠肝细胞线粒体MDA及超氧阴离子生成量明显减少,但SOD及GSH－Px不增加;血清中MDA减少,而GSH－Px及SOD增多。结论：在内霉素血症的发病机制中存在由于肝细胞线粒体氧自由基生成增加及其所引发的脂质过弧应增强所造成的氧化损伤,表明肝细胞线粒体的损伤在其发病机制中的重要作用,中药912液可以提高肝细胞线粒的抗氧化潜能,具有保护肝细胞的作用。     

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。