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11.
长期运动对增龄大鼠血浆胸主动脉内皮素-1的影响 总被引：3，自引：0，他引：3
为探讨长期不同持续时间和频率的游泳运动对增龄大鼠血浆、胸主动脉ET-1分泌的影响,选取2月龄雄性SD大鼠作为青年安静对照组,9-10月龄大鼠作为增龄组。增龄组又分为安静对照组和运动组,运动方式为无负重游泳,运动时间分别为每次1h和2h,运动频率为每周6次和3次,游泳运动周数总计14周。采用放免方法测定血浆、胸主动脉ET-1浓度。结果:⑴增龄时血浆ET-1的变化没有显著性;而胸主动脉ET-1随着增龄而升高(P<0 01)。⑵不同游泳运动后增龄大鼠血浆ET-1有升高的趋势,但差异无统计学意义,运动组之间的差异也没有显著性;运动后,胸主动脉ET-1的含量均下降(P<0 01)。结论:①增龄时胸主动脉ET-1水平明显升高,可能与增龄导致的内皮细胞损伤有关;增龄时血浆ET-1水平没有变化,提示血浆ET-1浓度不能准确地反应胸主动脉ET-1水平;②当增龄诱导的胸主动脉ET-1明显升高时,运动可以有效地降低其浓度,从而减弱ET-1的致病作用;③运动后各组血浆ET-1浓度适度升高可能有助于加强心肌收缩力。 相似文献
12.
目的：观察复肾口服液对阿霉素肾病大鼠肾脏的形态学影响。方法：采用尾静脉一次性注射阿霉素（ADR）复制肾病综合征模型。用光学显微镜、电子显微镜观察肾小球毛细血管、上皮细胞、基底膜及肾小管的病理形态学改变。结果：复肾口服液能使阿霉素肾病大鼠蛋白尿显著降低，肾小管管腔内的蛋白管型明显减少，肾小球淤血及上皮细胞和基底膜的损伤程度明显减轻，肾小球上皮细胞足突融合明显改善。结论：复肾口服液可促进肾病大鼠肾小球上皮细胞的修复及滤过膜功能的恢复，但存在着量效依赖关系。 相似文献
13.
48只28±2d清洁级SD大鼠,随机分为对照组和试验Ⅰ、Ⅱ组,每组16只,雌雄各半,分别饮用添加0、160和320 mg/L硼的蒸馏水2个月.试验结束时,大鼠10%水合氯醛腹腔麻醉,立即解剖取舌体,制作石蜡切片,HE染色,Olympus显微摄影系统观察并摄影.结果显示,试验Ⅰ组舌黏膜丝状乳头低矮且数量减少;菌状乳头较低矮,味蕾结构正常.试验Ⅱ组舌黏膜的损伤较为明显,丝状乳头数量明显减少,多数顶部钝圆,少数顶部溶解消失;菌状乳头低矮、狭小,味蕾体积变小、结构模糊,味蕾细胞排列稀疏,结构模糊.结果表明,高硼饮水对大鼠舌黏膜的组织结构与功能有一定的不良影响甚至明显的损伤作用. 相似文献
14.
Mukesh Nandave Ipseeta Mohanty T. C. Nag Shreesh Kumar Ojha Rajan Mittal Santosh Kumari Dharamvir Singh Arya 《Indian journal of clinical biochemistry : IJCB》2007,22(1):22-28
The present study evaluated the cardioprotective potential of vitamin-E by studying its effect on hemodynamic parameters,
lipid peroxidation, myocyte injury marker and ultrastructural changes in model of isoproterenol-induced myocardial necrosis
in rats. Wistar albino male rats (150–200 g) were randomly divided into saline, ISP control, and vit E groups. Vitamin E group
was administered vitamin E at a dose of 100mg/kg/day while saline and ISP control groups received saline orally for one month.
On 29th and 30th day, ISP (85 mg/kg, sc) was administered at an interval of 24 h to vit E and ISP control rats. On 31st day, rats of all groups were anesthetized and hemodynamic parameters were recorded. At the end of experimentation, animals
were sacrificed; hearts were excised and processed for biochemical and ultrastructural studies. ISP administration produced
marked cardiac necrosis as evidenced by significant decrease in my ocardial creatine kinase-MB as well as increase in malonaldialdehyde
levels. ISP-induced myocardial necrosis resulted in myocardial dysfunction as evidenced by significant depression in heart
rate and mean arterial pressure in the ISP control group as compared to saline control. Salient ultrastructural changes including
extensive loss of myofibrils, muscle necrosis, loss of mitochondria, and formation of several intracytoplasmic vacuoles and
lipid droplets further confirmed the ISP-induced myocardial damage. However, subsequent to ISP challenge, vit E treatment
significantly preserved the myocardium by restoring myocardial CK-MB activity, inhibiting the ISP-induced lipid peroxidation
and ultrastructural changes. Additionally, pre-and co-treatment of vit E prevented the deleterious ultrastructural changes
caused by ISP. These beneficial effects of chronic vit E treatment also translated into significant restoration of the altered
hemodynamic parameters. The present study clearly demonstrated the cardioprotective potential of vit E at dose of 100 mg/kg
in ISP-induced model of myocardial necrosis in rats. The significant restoration of altered hemodynamic parameters, myocardial
CK-MB activity, prevention of ISP-induced rise in lipid peroxidation and ultrastructural changes may confirm its cardioprotective
effect. 相似文献
15.
To investigate the inhibiting effect of β-Aescin on nuclear factor-κB (NF-κB) activation and the expression of tumor necrosis factor-α (TNF-α) protein after traumatic brain injury (TBI) in the rat brain, 62 SD rats were subjected to lateral cortical impact injury caused by a free-falling object and divided randomly into four groups: (1) sham operated (Group A); (2) injured (Group B); (3) β-Aescin treatment (Group C); (4) pyrrolidine dithocarbamate (PDTC) treatment (Group D). β-Aescin was administered in Group C and PDTC treated in Group D immediately after injury. A series of brain samples were obtained directly 6h, 24 h and 3 d respectively after trauma in four groups. NF-κB activation was examined by Electrophoretic Mobility Shift Assay (EMSA); the levels of TNF-α protein were measured by radio-immunoassay (RIA); the water content of rat brain was measured and pathomorphological observation was carried out. NF-κB activation, the levels of TNF-α protein and the water content of rat brain were significantly increased (P＜0.01) following TBI in rats. Compared with Group B, NF-κB activation (P＜0.01), the levels of TNF-α protein (P＜0.01) and the water content of brain (P＜0.05) began to decrease obviously after injury in Groups C and D.β-Aescin could dramatically inhibit NF-κB activation and the expression of TNF-α protein in the rat brain, alleviate rat brain edema, and that could partially be the molecular mechanism by which β-Aescin attenuates traumatic brain edema. 相似文献
16.
Yuan Yuan Fei Li Yue-min Wang Rong-qing Zhang Li-ping Wei Hai-chang Wang 《Journal of Zhejiang University. Science. B》2009,10(5):391-394
To shorten operation time and improve survival rate of rats with myocardial ischemia or myocardial infarction, we use a novel device comprised of a face mask and a head/neck retainer in this study. We report the basic design of the novel respiratory face mask (RFM) and evaluate its performance in a rat model of myocardial ischemia. The device is cost-effective and easier to handle than other devices, such as tracheal intubation. Compared with conventional tracheal intubation, we found that RFM shortens operation time significantly while keeping blood indices normal; the mean operation time for rats in the mask group was (32±3) min, and that for the intubation group was (45±7) min (P<0.05). Moreover, the size and shape of the RFM can be changed according to the body weight of rats. In conclusion, RFM is an appropriate device for the establishment of myocardial infarction or ischemia-reperfusion in rats. 相似文献
17.
GM1 stabilizes expression of NMDA receptor subunit 1 in the ischemic hemisphere of MCAo／reperfusion rat 总被引：3，自引：0，他引：3
Liu JR Ding MP Wei EQ Luo JH Song Y Huang JZ Ge QF Hu H Zhu LJ 《Journal of Zhejiang University. Science. B》2005,6(4):254-258
INTRODUCTION GM1 ganglioside (GM1) is the main kind ofgangliosides in mammalia, and most abundant inbrain tissue (Duchemin et al., 2002). It was reportedthat GM1 could protect cerebral ischemia in vivo andin vitro, one protective mechanism of which is thatGM1 could reduce neural injury induced by toxicityof excitatory amino acid via N-methyl-D-aspartate receptor (NMDAR) (Kharlamov et al., 1993; Simon et al., 1993; Garofalo and Cue… 相似文献
18.
大鼠酒精性肝损伤模型制作研究 总被引：1，自引：0，他引：1
目的 :为治疗酒精性肝病(AlcholicLiverDisease,ALD)筛选有效治疗药物提供依据。方法 :48只Wistar大鼠随机分成正常对照组(饮水)、模型Ⅰ组(饮 1 0 %酒)、模型Ⅱ组 (饮 1 5 %酒)、模型Ⅲ组 (饮 2 0 %酒 )。定期称重 ,静脉取血测定ALT(谷丙转氨酶 )、MDA(丙二醛 )、SOD(过氧化物歧化酶)、A/G(血浆白蛋白与球蛋白比值 )等指标。结果 :模型组在 4、8周与对照组比较ALT显著升高(P<0 .0 1 ) ,A/G显著降低 (P <0 .0 1 ) ,MDA含量明显升高 (P <0 .0 1 )。肝肿大 ,脂肪变性。镜下 :间质有炎性细胞浸润 ,肝索排列紊乱。小计量相对轻。结论 :大鼠饮用 2 0 %酒精 8周后 ,乙醇代谢的毒物直接作用于肝细胞使膜结构破坏[1 ] ,肝功能受到损伤 ,与人类酒精性肝病患者表现相同 ,因此 ,饮用乙醇法复制酒精性肝损伤模型是成功的。 相似文献
19.
运动及芦荟干预对糖尿病大鼠肝脏SOD活性及基因表达的影响 总被引：4，自引：0，他引：4
探讨运动及芦荟干预对糖尿病大鼠肝脏SOD活性及其基因表达的影响,为糖尿病非药物疗法提供理论依据。方法:建立糖尿病大鼠模型并分别给予运动、芦荟及运动芦荟等干预,8wk后分别用分光光度法及RT-PCR技术检测大鼠肝脏MnSOD、CuZnSOD活性及其基因表达。结果:运动、芦荟及运动芦荟三种干预方法均能显著提高大鼠肝脏MnSOD、CuZnSOD活性及MnSOD基因表达,其中运动芦荟组对糖尿病大鼠肝脏SOD活性及基因表达最为明显。结论:说明运动结合芦荟干预更能提高糖尿病大鼠肝脏SOD的活性及基因表达水平,促进肝脏抗氧化作用效果显著。 相似文献
20.
《运动与健康科学(英文)》2014,3(3):189-195
BackgroundExercise-associated menstrual dysfunction (EAMD) is a common health problem in female athletes as a part of female athlete triad (FAT), a condition related to low energy availability. In this study, we explored the possibility that carbohydrate supplements can improve the status of EAMD and prevent exercise-induced ovarian injury in a FAT rat model. This research aimed to provide experimental evidence with regard to the relationship of energy intervention and EAMD.MethodsForty-five female Sprague–Dawley rats (2 months old) were randomly divided into five experimental groups: control group (C), 9-week exercise as model for EAMD (E), post-EAMD recovery group (R), oligosaccharide intervention group (O), and glucose intervention group (G). All rats were sacrificed at the end of 9 weeks. Serum samples were collected for measuring gonadotropin releasing hormone, follicle stimulating hormone, luteinizing hormone, 17β-estradiol and progesterone levels. The ovaries were taken for investigation of exercise- and carbohydrate-induced follicular subcellular structure changes.ResultsExercise induced irregular menstrual cycles and ovary subcellular structural damages, such as swollenness of mitochondria in rats from groups E and R. Both glucose and oligosaccharide supplements restored well-differentiated mitochondria in the ovarian follicular cells, and a significant improvement of endoplasmic reticulum and Golgi in swollenness in theca cells in groups O and G compared to groups C, E, and R. There was no difference in mitochondria subcellular structural changes between groups O and G. Group E showed attenuation of serum levels of 17β-estradiol and progesterone compared to C. There were no differences of 17β-estradiol serum levels among groups O, G, and R, while group G showed a lower level of progesterone than C.ConclusionFemale adult rats with 9-week continuous exercise can cause menstrual dysregulation as a model for EAMD. Post-EAMD intervention with glucose and oligosaccharide intake can normalize the menstrual cycle, restore the follicular subcellular structure, and reverse the exercise-induced reduction of ovary sex hormones. It suggests a positive feedback of hypothalamus–pituitary–ovary axis might be involved in the molecular mechanisms of energy intake in treating EAMD. 相似文献