猴头菇对小鼠抗疲劳作用的实验研究

分别以猴头菇干粉（猴头菇Ⅰ组）和猴头菇浸出液（猴头菇Ⅱ组）饲喂小鼠,观察猴头菇对小鼠血清乳酸脱氢酶（ＬＤＨ）活力、血乳酸、血清尿素氮（ＢＵＮ）、肝糖原、肌糖原含量及运动耐力的影响。结果表明：实验６０ｄ后,猴头菇Ⅰ、Ⅱ组ＬＤＨ活力、肝糖原及肌糖原含量明显高于对照组（Ｐ＜０．０５或Ｐ＜０．０１）;运动后血乳酸的水平和ＢＵＮ的增量明显低于对照组（Ｐ＜０．０５或Ｐ＜０．０１）;运动后血乳酸消除速率显著高于对照组（Ｐ＜０．０５）;在运动耐力测定时在水中淹死的时间比对照组长得多（Ｐ＜０．０５）。提示：猴头菇具有明显的增强运动能力和解除疲劳的作用。     

肌酸对游泳大鼠乳酸、糖原含量和乳酸脱氢酶活性的影响

为探讨肌酸对提高大鼠运动能力的作用 ,观察了肌酸对游泳大鼠血清、心肌和骨骼肌乳酸、糖原含量和乳酸脱氢酶 (LDH)活性的影响。实验用雄性wistar大鼠 2 4只 ,随机分为正常组、游泳对照组和游泳补充肌酸组。两个游泳组每天游泳训练 1h,9天后 ,游泳 4h ,测定血清、心肌和骨骼肌乳酸水平 ,测定血清和骨骼肌乳酸脱氢酶活性以及心肌与骨骼肌糖原含量。结果显示 :肌酸可抑制游泳运动后大鼠血清、心肌和骨骼肌乳酸浓度以及血清LDH活性的升高幅度 ,抑制心肌和骨骼肌糖原含量及骨骼肌LDH活力的下降。以上结果表明 ,肌酸可改善运动后机体乳酸和糖原的代谢 ,降低运动性疲劳 ,提高大鼠的运动能力     

花生肽对小鼠的抗疲劳作用研究

目的：探讨花生肽对ICR小鼠的抗疲劳作用。方法：采用SPF级雄性ICR小鼠80只按体重随机分为4组,分别为空白对照组、3个花生肽干预组（250、500、1 000 mg/kg BW］。每日经口灌胃给予受试样品水溶液,干预周期为30 d,干预结束后进行负重游泳试验,并对各组小鼠负重游泳力竭时间进行记录,同时对其血糖水平、血清尿素氮含量及乳酸脱氢酶活力进行测定,并检测各组小鼠血乳酸水平,检测各组小鼠肝、肌糖原含量,并测定小鼠血清生化指标,同时测定小鼠心肌、肝脏及腓肠肌氧化应激和脂质过氧化指标水平。结果：与空白对照组相比,花生肽可显著延长小鼠负重游泳力竭时间,并提高其乳酸脱氢酶活性,降低运动后小鼠血乳酸含量,加强肌糖原储备,提高心肌SOD活力。结论：花生肽具备一定的抗疲劳作用。     

蚂蚁水提取物抗疲劳的研究

目的:研究蚂蚁水提取物抗疲劳作用及其机制,为提高运动员训练效果及比赛成绩提供科学方法。方法:将80只小鼠随机分为4组(n=20):阴性生理盐水对照组、蚂蚁水提取物分为高、中、低三个剂量组,比较各组小鼠力竭游泳时间、肝糖原、肌糖原、乳酸脱氢酶、超氧化物歧化酶、血乳酸和血尿素氮的差异,研究蚂蚁水提取物抗疲劳的效果和机制。结果:与阴性生理盐水对照组比较,蚂蚁水提取物中高剂量组能够延长小鼠负重游泳时间(P<0.01),提高小鼠乳酸脱氢酶、超氧化物歧化酶活力(P<0.01),降低血乳酸和血尿素氮含量(P<0.01),提高小鼠肌糖原储备量,但对肝糖原的储备量影响不大。结论:蚂蚁水提取物能起到抗疲劳作用,其原因可能是它提高了乳酸脱氢酶、超氧化物歧化酶活力,使得代谢产物的分解加快,从而小鼠在耐力运动中坚持更久的时间。     

菟丝子对运动训练大鼠睾酮含量、物质代谢及抗运动疲劳能力的影响

本文以大强度耐力训练大鼠为模型,对菟丝子对运动训练大鼠睾酮含量、物质代谢及抗运动疲劳能力的影响进行了研究.试验中分别以1.16、2.32、6.96 g.kg-1.d-1的剂量给大鼠灌胃42d,并进行负重游泳实验、血清睾酮等生化指标测定.结果显示,菟丝子各剂量组力竭游泳时间长于运动对照组(T组)(P＜0.01);血清睾酮高于T组(P＜0.01),血清皮质酮低于T组(P＜0.05);各组间血清睾酮与皮质酮比值变化与睾酮变化较为一致;肝糖原(P＜0.05)、肌糖原(P＜0.01)高于T组;血清尿素氮低于T组(P＜0.05);血红蛋白高于T组(P＜0.05).从而表明补充菟丝子可以减轻大鼠血睾酮、皮质酮受高强度运动量的影响,维持在正常生理水平;促进蛋白质合成,抑制氨基酸和蛋白质分解,提高血红蛋白含量和糖原的储备,增强抗疲劳能力,具有多靶点、多途径的显著特点.     

海蛇乙醇浸出物对小鼠免疫系统的影响

目的 探讨海蛇乙醇浸出物（AEBFSS）在小鼠体内、体外对免疫系统的影响。方法 体外试验：采用AEBFSS与小鼠脾细胞共孵育72h,测定T、B淋巴细胞转化功能;体内试验：采用每天灌胃给予小鼠1次AEBFSS,共6天。测定脾脏中T淋巴细胞转化功能和溶血素抗体生成水平。结果 在体外条件下低浓度AEBFSS促进T、B淋巴细胞增殖,高浓度时则作用相反;在体内条件下低浓度AEBFSS能增加B细胞生成溶血素抗体,对T细胞增殖无明显影响,高浓度则抑制T、B细胞功能。结论 AEBFSS对小鼠免疫系统有一定的双向调节作用。     

条斑紫菜多糖抗疲劳生物活性研究

主要应用活体动物实验技术,研究了纯化产物紫菜多糖的抗疲劳作用及量效关系。通过紫菜多糖PY-G1不同剂量对小鼠游泳时间、乳酸脱氢酶活性、肌糖原和肝糖原含量等指标的检测,分析了紫菜多糖提高小鼠抗疲劳生物活性功能及其量效关系。实验结果表明,紫菜多糖可显著延长小鼠游泳时间,最高可以提高37%;并且可以使小鼠在游泳前后乳酸脱氢酶含量分别增加35%和37.5%(P<0.05);增加小鼠肌糖原储备量和肝糖原储备量,其肌糖原储备量和肝糖原储备量最高可以分别增加85.6%和86%。实验结果表明,条斑紫菜多糖具有明显提高小鼠抗疲劳生物学活性。     

狗在运动中的肌糖原消耗与无氧阈的关系

本实验测定了5条狗的无氧阈值,运动耐受时间、衰竭时的血乳酸浓度及运动中的肌糖原消耗量。结果如下:无氧阈值,1.与运动耐受时间呈正相关(r=0.947,P<0.02);2.与运动中肌糖原消耗量呈负相关(r=-0.959,P<0.01);3.与衰竭时的血乳酸浓度呈负相关(r=-0.942,P<0.02)。实验结果提示,无氧阈值是反映机体耐力的可靠指标。而运动中肌糖原消耗少,血乳酸积累程度轻,可能是无氧阈值之所以能够反映机体耐力的物质基础。     

黄芪多糖抗小鼠疲劳的作用机制研究

目的:探讨黄芪多糖对小鼠的抗疲劳作用及机制。方法:该研究分为实验组和对照组两组,实验组设置三组剂量0.2,0.05,0.0125 g/kg对小鼠连续灌胃28天,对照组给予蒸馏水灌胃,进行负重游泳试验计算游泳力竭时间,并检测小鼠全血中血糖,血中乳酸含量,肝脏超氧化物歧化酶(SOD)、丙二醛(MDA)、乳酸脱氢酶(LDH)含量及肌组织中糖原储备量。结果:1).与对照组相比较,黄芪多糖低剂量、高剂量组小鼠负重游泳时力竭时间明显延长;2).中剂量组小鼠运动后肝脏SOD活力值比对照组明显增高,高剂量组肌糖原的储存量明显升高,而低剂量组乳酸明显降低。结论:黄芪多糖具有抗疲劳作用,可能通过增加抗氧化酶类SOD活性、减少乳酸的产生及增加肌糖原能量储存等途径起作用。     

力竭性运动后鲇鱼幼鱼乳酸、糖原和葡萄糖水平的变动

于(25±1)℃的条件下分别测定了鲇鱼(Silurus asotusLinnaeus)幼鱼静止状态(对照组)与力竭性运动后不同恢复时间(0、0.5、1、2、48、、16h)肌肉、血液和肝脏三种组织中乳酸、糖原和葡萄糖的含量水平。结果显示:鲇鱼幼鱼力竭性运动后肌乳酸和血乳酸水平迅速上升并即刻达到峰值(12.13±0.19)μmol/g和(4.57±0.23)mmol/L,而肝乳酸的峰值((9.78±0.69)μmol/g)却出现在运动后恢复1h;肌组织乳酸的迅速上升伴随着糖原的快速下降,葡萄糖含量保持相对稳定;肌乳酸恢复历时为8h,清除速率为0.9μmol/h.g。实验结果表明鲇鱼力竭性运动后存在着明显的"乳酸泄露"现象,其无氧代谢的底物主要是糖原;肝组织可能是一个乳酸的临时贮存库。     

Increased liver glycogen levels enhance exercise capacity in mice

Muscle glycogen depletion has been proposed as one of the main causes of fatigue during exercise. However, few studies have addressed the contribution of liver glycogen to exercise performance. Using a low-intensity running protocol, here, we analyzed exercise capacity in mice overexpressing protein targeting to glycogen (PTG) specifically in the liver (PTG^OE mice), which show a high concentration of glycogen in this organ. PTG^OE mice showed improved exercise capacity, as determined by the distance covered and time ran in an extenuating endurance exercise, compared with control mice. Moreover, fasting decreased exercise capacity in control mice but not in PTG^OE mice. After exercise, liver glycogen stores were totally depleted in control mice, but PTG^OE mice maintained significant glycogen levels even in fasting conditions. In addition, PTG^OE mice displayed an increased hepatic energy state after exercise compared with control mice. Exercise caused a reduction in the blood glucose concentration in control mice that was less pronounced in PTG^OE mice. No changes were found in the levels of blood lactate, plasma free fatty acids, or β-hydroxybutyrate. Plasma glucagon was elevated after exercise in control mice, but not in PTG^OE mice. Exercise-induced changes in skeletal muscle were similar in both genotypes. These results identify hepatic glycogen as a key regulator of endurance capacity in mice, an effect that may be exerted through the maintenance of blood glucose levels.     

Effects of Pulse Current on Endurance Exercise and Its Anti-Fatigue Properties in the Hepatic Tissue of Trained Rats

Fatigue is synonymous with a wide spectrum of familiar physiological conditions, from pathology and general health, to sport and physical exercise. Strenuous, prolonged exercise training causes fatigue. Although several studies have investigated the effects of electrical stimulation frequency on muscle fatigue, the effects of percutaneous pulse current stimulation on fatigue in the hepatic tissue of trained rats is still unclear. In order to find an effective strategy to prevent fatigue or enhance recovery, the effects of pulse current on endurance exercise and its anti-fatigue properties in exercised rats were studied. Rats were subjected to one, three or five weeks of swimming exercise training. After exercise training, rats in the treated group received daily applications of pulse current. All rats were sacrificed after one, three or five weeks of swimming exercise, and the major biochemical indexes were measured in serum and liver. The results demonstrate that pulse current could prolong the exhaustion swimming time, as well as decrease serum ALT, AST and LD levels and liver MDA content. It also elevated serum LDH activity, liver SOD activity and glycogen content. Furthermore, pulse current increased the expression of Bcl-2 and decreased the expression of Bax. Taken together, these results show that pulse current can elevate endurance capacity and facilitate recovery from fatigue.     

大豆卵磷脂对小鼠的抗疲劳和抗氧化作用研究

目的：研究大豆卵磷脂的抗疲劳及抗氧化作用。方法：小鼠经口给予大豆卵磷脂30天后,采用负重游泳实验,观察记录小鼠游泳死亡时间;检测血清尿素氮、肝糖原;测定血清和肝匀浆超氧化物歧化酶（SOD）活性、谷胱甘肽过氧化物酶（GSH—Px）活力、丙二醛（MDA）含量。结果：给予大豆卵磷脂后,与对照组相比,实验组小鼠负重游泳时间明显延长,肝糖原消耗量减少,降低运动后血清尿素氮水平（P〈0．05）;升高小鼠血清和肝匀浆SOD活性及GSH-Px活力,降低MDA的含量（P〈0．05）。结论：大豆卵磷脂具有抗疲劳和抗氧化作用。     

Effect of the nucleotides CMP and UMP on exhaustion in exercise rats

The aetiology of muscle fatigue has yet not been clearly established. Administration of two nucleotides, cytosine monophosphate (CMP) and uridine monophosphate (UMP), has been prescribed for the treatment of neuromuscular affections in humans. Patients treated with CMP/UMP recover from altered neurological functions and experience pain relief, thus the interest to investigate the possible effect of the drug on exhausting exercise. With such aim, we have determined, in exercised rats treated with CMP/UMP, exercise endurance, levels of lactate, glucose and glycogen, and the activity of several metabolic enzymes such as, creatine kinase (CK), lactate dehydrogenase (LDH), and aspartate aminotransferase (AST). Our results show that rats treated with CMP/UMP are able to endure longer periods of exercise (treadmill-run). Before exercise, muscle glucose level is significantly higher in treated rats, suggesting that the administration of CMP/UMP favours the entry of glucose in the muscle. Liver glycogen levels remains unaltered during exercise, suggesting that CMP/UMP may be implicated in maintaining the level of hepatic glycogen constant during exercise. Lactate dehydrogenase and aspartate aminotransferase activity is significantly lower in the liver of treated rats. These results suggest that administration of CMP/UMP enable rats to endure exercise by altering some metabolic parameters.     

Ebselen reduces hyperglycemia temporarily-induced by diazinon: a compound with insulin-mimetic properties

The present study investigated the effect of ebselen (EB) against hyperglycemia induced by the organophosphate (OPI) diazinon (DI) in rats. The insulin-mimetic properties of EB were investigated in vitro with the aim of better understanding the hypoglycemic effect of this compound. The protective effect of EB against pancreatic and hepatic damage caused by DI in rats was also appraised. In the in vivo experiments, rats were pre-treated with a single injection of EB (50mg/kg, intraperitoneal, i.p.). Afterward, animals were treated with a single injection of DI (200 mg/kg, i.p.). The parameters indicative of pancreatic and hepatic damage such as, serum amylase, lipase, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) activities as well as serum glucose levels, hepatic glycogen content and glucose-6-phosphatase (G6Pase) activity were determined. EB pre-treatment was effective in reducing serum amylase, lipase, AST, ALT, ALP, and LDH activities, protecting against pancreatic and hepatic damage. EB reduced hyperglycemia and increased hepatic glycogen content in animals exposed to DI. In the in vitro assays, EB (150 μM) or insulin (IN 10 μM, positive control) was incubated with either skeletal muscle or hepatic tissue with the aim of measuring glucose uptake, glycogen synthesis and glycogen breakdown. EB increased the glucose uptake in skeletal muscle, stimulated hepatic glycogen synthesis and inhibited glycogen breakdown in a similar way to IN. In conclusion, EB, possibly through its insulin-mimetic action, protected against pancreatic and hepatic damage caused by DI in rats.     

Hypoglycemic action of the pectin present in the juice of the inflorescence stalk of plantain (Musa sapientum)—Mechanism of action

The pectin isolated from the juice of the inflorescence stalk of plantain (Musa sapientum) has been found to show significant hypoglycemic effect both in normoglycemic and alloxan diabetic rats. After its administration at a dose of 20mg/100g body weight, there was increase in the concentration of hepatic glycogen, increased glycogenesis as evident from the increased activity of glycogen synthetase and in normoglycemic rats increased incorporation of labelled glucose into hepatic glycogen. Glycogenolysis and glyconeogenesis were lower as was evident from the decreased activity of glycogen phosphorylase and gluconeogenic enzymes.     

Characterization of the in vitro kinase activity of a partially purified soluble GST/JAK2 fusion protein

In vivo effects of insulin and vanadium treatment on glycogen synthase (GS), glycogen synthase kinase-3 (GSK-3) and protein phosphatase-1 (PP1) activity were determined in Wistar rats with streptozotocin (STZ)-induced diabetes. The skeletal muscle was freeze-clamped before or following an insulin injection (5 U/kg i.v.). Diabetes, vanadium, and insulin in vivo treatment did not affect muscle GSK-3 activity as compared to controls. Following insulin stimulation in 4-week STZ-diabetic rats muscle GS fractional activity (GSFA) was increased 3 fold (p < 0.05), while in 7-week diabetic rats it remained unchanged, suggesting development of insulin resistance in longer term diabetes. Muscle PP1 activity was increased in diabetic rats and returned to normal after vanadium treatment, while muscle GSFA remained unchanged. Therefore, it is possible that PP1 is involved in the regulation of some other cellular events of vanadium (other than regulation of glycogen synthesis). The lack of effect of vanadium treatment in stimulating glycogen synthesis in skeletal muscle suggests the involvement of other metabolic pathways in the observed glucoregulatory effect of vanadium.     

Effect of the acclimation to high environmental temperature on the activity of hepatic glycogen phosphorylase (a+b and a), liver glycogen content and blood glucose level in rats

(1) Changes in the activity of hepatic glycogen phosphorylase a+b and a (GPh-ase a+b and a), liver glycogen content and blood glucose level during acclimation to moderate high environmental temperature (35±1 °C) were studied. (2) Experiments were carried out on adult fed Wistar rats of both sexes, previously given either short-term (1, 4 and 7 days) or long-term (14, 21, 30 and 60 days) exposure to high environmental temperature. The controls were continuously kept at room temperature (20±2 °C). (3) The results obtained showed that in the period of short-term exposure the liver glycogen content was decreased significantly (after the first and fourth days in male rats and after first day in female rats) and the GPh-ase a activity increased (after first day in male rats and after first, fourth and seventh day in female rats). Long-term exposure caused significant increased liver glycogen content (beginning from the 14th day in male rats and the 21st day in female rats) until the end of the acclimation period (60 days). The elevated activity of GPh-ase a persists after 14th day of exposure only in female rats while there are no significant changes over the rest of the acclimation period in both sexes. There were no significant changes in total GPh-ase activity during the whole period of exposure. Blood glucose level was significantly decreased throughout the whole period of acclimation to high environmental temperature, in both sexes (except in the 1 day exposed groups). (4) The increased activity of hepatic GPh-ase a and decreased glycogen content suggested that the short-term exposure to heat stimulates the glycogenolytical processes. Decreased blood glucose level, and elevated liver glycogen content (r=-0.7467 in male and r=-0.6548 in female rats) suggested that prolonged exposure to high environmental temperature stimulated glycogenogenesis, without changes in the GPh-ase activity.