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21.
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   
22.
The study was undertaken to evaluate the possible involvement of oxidative stress in the pathogenesis of ethanol induced testicular atrophy in rats. Adult male rats were orally administered ethanol at a dose of 1.6 g/kg body weight/day for four weeks. Twenty-four hours after the last treatment the rats were sacrificed using anesthetic ether. Testes were removed and weighed. Apoptosis was studied by using the Feulgen reaction on 5 μ thin paraffin sections of testis. Testicular homogenate was prepared and centrifuged. The supernatant was used for the estimation of extent of lipid peroxidation and antioxidant defense status. There was significant reduction in body weight: and in testicular weight and diameter in ethanol treated rats. Extent of germ cell apoptosis was significantly high in ethanol treated rats. Ethanol treated rats showed significantly high tissue TBARS level and glutathione S-transferase activity; and low tissue ascorbic acid, reduced glutathione, superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase activities. Chronic ethanol administration resulted in high oxidative stress in the testes either due to increased extent of lipid peroxidation or due to decreased antioxidant defenses, and thereby induces germ cell apoptosis leading to testicular atrophy.  相似文献   
23.
Objective: To investigate the protective effects and mechanisms of action of dexamethasone and Salvia miltiorrhiza on multiple organs in rats with severe acute pancreatitis (SAP). Methods: The rats were divided into sham-operated, model control, dexamethasone treated, and Salvia miltiorrhiza treated groups. At 3, 6, and 12 h after operation, the mortality rate of different groups, pathological changes, Bcl-2-associated X protein (Bax) and nuclear factor-κB (NF-κB) protein expression levels in multiple organs (the pancreas, liver, kidneys, and lungs), toll-like receptor 4 (TLR-4) protein levels (only in the liver), intercellular adhesion molecule 1 (ICAM-1) protein levels (only in the lung), and terminal deoxynucleotidy transferase mediated deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL) staining expression levels, as well as the serum contents of amylase, glutamate-pyruvate transaminase (GPT), glutamic-oxaloacetic transaminase (GOT), blood urea nitrogen (BUN), and creatinine (CREA) were observed. Results: The mortality rate of the dexamethasone treated group was significantly lower than that of the model control group (P<0.05). The pathological changes in multiple organs in the two treated groups were relieved to different degrees (P<0.05 and P<0.01, respectively), the expression levels of Bax and NF-κB proteins, and apoptotic indexes of multiple organs were reduced (P<0.05 and P<0.01, respectively). The contents of amylase, GPT, GOT, BUN, and CREA in the two treated groups were significantly lower than those in model control groups (P<0.05 and P<0.01, respectively). The expression level of ICAM-1 protein in the lungs (at 3 and 12 h) in the dexamethasone treated group was significantly lower than that in the Salvia miltiorrhiza treated group (P<0.05). The serum contents of CREA (at 12 h) and BUN (at 6 h) of the Salvia miltiorrhiza treated group were significantly lower than those in the dexamethasone treated group (P<0.05). Conclusions: Both dexamethasone and Salvia miltiorrhiza can reduce the inflammatory reaction, regulate apoptosis, and thus protect multiple organs of rats with SAP.  相似文献   
24.
This study aimed to elucidate the mechanisms of melatonin to manage neurological damage in Alzheimer’s disease (AD) induced in ovariectomized rats. Forty adult female rats were enrolled in our study and were classified as; gonad intact control, ovariectomized control group, ovariectomized rats received melatonin, ovariectomized rats injected with AlCl3 to induce AD and AD-induced rats treated with melatonin. Hydrogen peroxide (H2O2), malondialdehyde (MDA), total antioxidant capacity (TAC), superoxide dismutase (SOD), catalase (CAT), B cell lymphoma 2 (Bcl-2), brain derived neurotrophic factor (BDNF), acetylcholinesterase (AchE) and acetylcholine (Ach) were estimated in the brain tissues of the different groups. Treatment of AD-induced rats with melatonin produced marked improvement in the most studied biomarkers which was confirmed by histological investigation of the brain. In Conclusion, melatonin significantly ameliorates the neurodegeneration characteristic of AD in experimental animal model due to its antioxidant, antiapoptotic, neurotrophic and anti-amyloidogenic activities.  相似文献   
25.
目的:研究有氧运动对糖尿病肾病(DN)大鼠降钙素基因相关肽(CGRP)的影响。方法:链脉佐菌素(STZ)诱导糖尿病大鼠模型,随机分为糖尿病组(D)、糖尿病运动组(D+E)、同时另设正常对照组(N),有氧运动干预10周后,测定空腹血糖(FBG)、尿微量白蛋白(U-mAIb)、血浆和肾脏组织中内皮素(ET)和CGRP含量。结果:糖尿病大鼠U-mAIb增加,ET升高,CGRP下降,运动干预10周后,D+E组DN大鼠U-mAIb较D组显著降低,ET显著下降,CGRP明显升高。结论:有氧运动对糖尿病大鼠肾脏病变有一定的保护作用,其部分机制可能是通过上调CGRP含量而实现的。  相似文献   
26.
通过运用实验法和数理统计法研究不同运动方式对各周龄大鼠的影响,说明大鼠体内丙酮酸含量的变化情况。结果发现:大鼠在递增负荷的情况下,各周龄的大鼠体内丙酮酸的含量会有一定的变化;周龄越高,产生丙酮酸的量相对较少,这可能与大鼠机体代谢率有关。  相似文献   
27.
研究表明运动能力与肝脏的生理机能密切相关。运动后理气扶正中药与运动训练相结合,有助于稳定肝抗氧化酶活性,并促进抗氧化酶活性的恢复。本研究将大鼠分为安静和运动两大组。让运动组大鼠在跑台上进行递增负荷运动建立低血色素大鼠模型,安静组为对照。各组大鼠又分为喂水和喂中药两类,喂水大鼠为喂中药大鼠的对照。通过测试大鼠红细胞计数、血红蛋白、红细胞比积以及肝脏组织的抗氧化酶的活性和自由基代谢产物含量的变化,以了解运动对血色素下降和自由基代谢的影响以及中药干预对血色素下降和自由基代谢的作用。  相似文献   
28.
梗阻性黄疸大鼠肝脏损害及血清毒性物质变化   总被引:1,自引:0,他引:1  
目的:探讨梗阻性黄疸(梗黄)大鼠肝脏损害及其血清毒性物质的变化。方法:采用胆总管结扎方法建立梗阻性黄疸大鼠模型,将36只大鼠随机分为假手术(sham)组6只、梗阻性黄疸(CBDL)组30只(CBDL组又分为1周、2周、3周、4周、5周亚组,每组6只)。监测各组血液TNF-α、内毒素、肝功能变化。结果:CB—DL组均可见肝细胞坏死及增生,汇管区可见胆管扩张、胆汁淤积,肝组织改变随梗阻时间的延长而逐渐加重,血清内毒素及TNF-α含量与梗阻时间明显相关。结论:CBDL大鼠肝脏形态改变明显,血ALT、TBIL、内毒素、TNF-α含量明显升高,并与梗黄时间有关。  相似文献   
29.
目的:探讨高血压大鼠左室流出道自发性慢反应电位0相和4相去极离子流中Ca2 的作用.方法:利用自发性高血压大鼠(SHR)的离体心脏,常规玻璃微电极细胞内记录方法和Ca2 离子通道阻断剂维拉帕米(VER),观测最大舒张电位(MDP)、0相除极幅度(APA)、0相最大除极速度(Vmax)、4相自动除极速度(VDD)、复极50%(APD50)和90%(APD90)的时间以及自发放电频率(RPF).结果:1.0μmol/L维拉帕米可使该慢电位的APA、Vmax、VDD明显减小,RPF减慢(P<0.01);APD、APD90延长(P<0.05).结论:(1)该区域的自发慢电位0相去极离子流主要为Ca2 内流.(2)4相去极离子流中,Ca2 内流起部分作用.  相似文献   
30.
BackgroundOsteoarthritis (OA) is a form of arthritis due to degradation of articular cartilage. OA is associated with stiffness, joint pain, and dysfunction, affecting adults worldwide. Galangin is a bioactive flavonoid that exerts several therapeutic and biological activities. Anti-hyperglycemic, anti-inflammatory, anti-cancer, and anti-apoptotic activities of galangin have been reported in several studies. In the present study, rats were divided into normal control, OA (control), galangin 10 mg/kg (low-dose), galangin 100 mg/kg (high-dose), and celecoxib 30 mg/kg (positive control) groups. All doses were administered orally for 14 consecutive days. The urinary type II collagen (µCTX-II) level as well as reactive oxygen species, tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, superoxide dismutase, catalase, lipid peroxidation, reduced glutathione, and glutathione peroxidase levels were measured. In addition, the CTX-II mRNA and protein expression levels were measured.ResultsGalangin supplementation significantly reduced the µCTX-II level compared with controls. Galangin treatment significantly reduced reactive oxygen species, lipid peroxidation, interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha levels, but increased catalase, superoxide dismutase, glutathione peroxidase, and reduced glutathione levels. Galangin treatment significantly reduced the CTX-II mRNA and protein expression levels. The low CTX-II level in tissue indicated the inhibition of cartilage degradation.ConclusionsIn summary, supplementation with galangin was effective against OA. The identification of potential therapeutic agents that inhibit inflammation may be useful for the management and prevention of OA.How to cite: Su Y, Shen L, Xue J, et al. Therapeutic evaluation of galangin on cartilage protection and analgesic activity in a rat model of osteoarthritis. Electron J Biotechnol 2021;53. https://doi.org/10.1016/j.ejbt.2021.05.005  相似文献   
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