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1.
力竭性运动后骨骼肌、心肌线粒体超微结构可发生体积增大、基质电子密度下降、嵴断裂及空泡样等退行性可逆改变。  相似文献   
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Background: Edaravone had been validated to effectively protect against ischemic injuries. In this study, we investigated the protective effect of edaravone by observing the effects on anti-apoptosis, regulation of Bcl-2/Bax protein expression and recovering from damage to mitochondria after OGD (oxygen-glucose deprivation)-reperfusion. Methods: Viability of PC 12 cells which were injured at different time of OGD injury, was quantified by measuring MTT (2-(4,5-dimethylthia-zol-2-yl)-2,5-diphenyltetrazolium bromide) staining. In addition, PC 12 cells' viability was also quantified after their preincubation in different concentration of edaravone for 30 min followed by (OGD). Furthermore, apoptotic population of PC 12 cells that reinsulted from OGD-reperfusion with or without preincubation with edaravone was determined by flow cytometer analysis, electron microscope and Hoechst/Pl staining. Finally, change of Bcl-2/Bax protein expression was detected by Western blot. Results: (1) The viability of PC12 cells decreased with time (1-12 h) after OGD. We regarded the model of OGD 2 h, then replacing DMEM (Dulbecco's Modified Eagle's Medium) for another 24 h as an OGD-reperfusion in this research. Furthermore, most PC 12 cells were in the state of apoptosis after OGD-reperfusion. (2) The viability of PC 12 cells preincubated with edaravone at high concentrations (1, 0.1, 0.01 μmol/L) increased significantly with edaravone protecting PC 12 cells from apoptosis after OGD-reperfusion injury. (3) Furthermore, edaravone attenuates the damage of OGD-reperfusion on mitochondria and regulated Bcl-2/Bax protein imbalance expression after OGD-reperfusion. Conclusion: Neuroprotective effects of edaravone on ischemic or other brain injuries may be partly mediated through inhibition of Bcl-2/Bax apoptotic pathways by recovering from the damage of mitochondria.  相似文献   
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The authors investigated the influence of green tea polyphenols (GTPs) on the liver mitochondria permeability transition pore (PTP) opening through mit ochondria swelling and change of mitochondria membrane potential. The data showe d that GTPs had obvious protective effect on the Ca2+-induced PTP opening in a d ose-dependent manner detected by mitochondria swelling. The results were obtain ed by measuring the change of mitochondria membrane potential through Rh 123. Further experiments were conducted to examine the detailed influence of GTP s on Ca2+import and export of mitochondria. The results showed that GTPs h ad rem arkably inhibitory effect on the Ca2+-induced Ca2+ import in mitoch ondria; and t hat they could accelerate Ca2+-release from mitochondria. Our data provid e an al ternate interpretation of the potent protective function of GTPs on cell against apoptosis.  相似文献   
5.
Oocyte quality has long been considered as a main limiting factor for in vitro fertilization (IVF). In the past decade,extensive observations demonstrated that the mitochondrion plays a vital role in the oocyte cytoplasm, for it can provide adenosine triphosphate (ATP) for fertilization and preimplantation embryo development and also act as stores of intracellular calcium and proapoptotic factors. During the oocyte maturation, mitochondria are characterized by distinct changes of their distribution pattern from being homogeneous to heterogeneous, which is correlated with the cumulus apoptosis. Oocyte quality decreases with the increasing maternal age. Recent studies have shown that low quality oocytes have some age-related dysfunctions, which include the decrease in mitochondrial membrane potential, increase of mitochondrial DNA (mtDNA) damages, chromosomal aneuploidies,the incidence of apoptosis, and changes in mitochondrial gene expression. All these dysfunctions may cause a high level of developmental retardation and arrest of preimplantation embryos. It has been suggested that these mitochondrial changes may arise from excessive reactive oxygen species (ROS) that is closely associated with the oxidative energy production or calcium overload,which may trigger permeability transition pore opening and subsequent apoptosis. Therefore, mitochondria can be seen as signs for oocyte quality evaluation, and it is possible that the oocyte quality can be improved by enhancing the physical function of mitochondria. Here we reviewed recent advances in mitochondrial functions on oocytes.  相似文献   
6.
解偶联蛋白3是线粒体内膜上的一种转运蛋白,研究证实解偶联蛋白3与线粒体能量代谢、线粒体活性氧生成及脂肪代谢等有关。就解偶联蛋白3的结构、分布、表达调控及其介导的线粒体活性氧生成等相关问题作一综述。  相似文献   
7.
Twenty four Wistar strain albino rats were used for the investigations. Lecithin 50 and 100 mg/kg b wt was administered for 1 week by oral route. Liver damage was induced by intra peritoneal administration of 400 mg/kg b wt d-galactosamine on the last day. At the end of the study animals were sacrificed and liver enzyme levels, histopathology, mitochondrial integrity, expression of p53, Bax and Bcl-2 mRNA levels were studied. Increases in the liver enzyme levels by d-GalN were significantly inhibited by pretreatment with lecithin. Histopathological observation further confirmed the hepatoprotective effect of lecithin. In addition, the disruption of mitochondrial membrane, up regulation of Bax and down regulation of Bcl-2 mRNA levels in the liver of d-GalN intoxicated rats were effectively prevented by pretreatment with lecithin. The results of the present study validate our conviction that d-GalN causes hepatic damage via mitochondrial pathway involving Bax and Bcl-2.  相似文献   
8.
运动与线粒体   总被引:6,自引:0,他引:6  
对近年来有关运动与线粒体的研究成果进行了深入分析,综述了不同运动状态下线粒体的呼吸机能、抗氧化能力、膜特性、mtDNA及形态结构等方面的变化,以及大鼠进行长期训练后及补充外源性物质后线粒体机能出现的良好性变化等。  相似文献   
9.
线粒体是细胞的动力工厂,是ATP的主要来源。合成ATP的动力是线粒体内膜内外的H^ 浓度差,由于H^ 的跨膜转运与电子的传递相偶联,因而还原当量的多少,细胞色素C的外溢,构成电子传递链的氧化还原酶的活性,均影响到电子的传递;线粒体膜的通透性的改变也直接影响到膜内外H^ 的浓度差。  相似文献   
10.
The great majority of genetic disorders are caused by defects in the nuclear genome. However, some significant diseases are the result of mitochondrial mutations. Because of the unique features of the mitochondria, these diseases display characteristic modes of inheritance and a large degree ofphenotypic variability. Recent studies have suggested that mitochondrial dysfunction plays a central role in a wide range of age-related disorders and various forms of cancer.  相似文献   
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