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1.
Objective: To construct a PC12 cell strain with neuronal differentiation, and observe the apoptosis and pro-liferation activity effects induced these cells by Amyloid beta-Protein (Aβ-43). Methods: 1) PC12 cells in logarithmicgrowth phase were subcultured for 24 h. After the culture fluid was changed, the cells were treated with Rat-β-NGF andcultured for 9 days. 2) Neuronal differentiation of PC12 cells in logarithmic growth phase were divided into four groups:control group (0), experimental group (1), experimental group (2) and experimental group (3). The concentrations of Aβ inthe four groups were 0 μmol/L, 1.25 μ mol/L, 2.5 μ mol/L and 5 μmol/L, respectively. The cells were harvested at 24, 48 and72 h later and stained with AnnexinV-FITC/PI after centrifugation and washing. Then flow cytometry was conducted toexamine the apoptosis percentage. 3) NGF-induced PC12 cells were selected and Aβ with different concentrations wasadded. The final concentrations of Aβ were 0 μmol/L, 1.25 μmol/L, 2.5 μmol/L and 5 μ mol/L, respectively. After the cellswere incubated in an atmosphere of 5% CO2 at 37 ℃ in an incubator for 72 h, the OD values were examined. Results: 1)Neuronal differentiated PC 12 cell lines were successfully established. 2) Flow cytometric examination indicated that Aβ(1.25, 2.5, and 5.0 μmol/L) could effectively induce apoptosis of neuronal-differented cells at the 24 h, 48 h and 72 h timepoints. 3) Aβ (0-5.00 μ mol/L) had no obvious effect on proliferation or restraining of the neuronal differentiation of thePC 12 cells after a 72 h interacting process. Conclusion: This investigation revealed successful neuronal differentiation of thePC12 cell strain. The induction of apoptosis of the neurocytes by various concentrations of Aβ was observed and the in-fluence of Aβ on induced proliferation of PC 12 cells by Rat-β-NGF was revealed. This study -05 provide basis for futureresearch on the molecular cure of AD and interdiction of AD evolution. 相似文献
2.
Winston Costa Pereira Muddanna S. Rao D. M. Vasudevan 《Indian journal of clinical biochemistry : IJCB》2003,18(2):161-168
Immunization with a proper dose of an antigenic stimulus leads to cell proliferation and antibody response of circulating
lymphocytes. We have previously observed that Secondary immunized spleenocytes resist ceramide-mediated apoptosisin vitro. Our present study is aimed at investigating thein vivo effect of immunization on apoptosis. Mice were subjected to either Primary or Secondary dose with Tetanus Toxoid. Unimmunized
spleenocytes served as controls. Unimmunized, Primary and Secondary immunized mice were later exposed to chemotherapeutic
drugs such as Etoposide/Methotrexate/Vincristine to induce apoptosis. Apoptosis was studied by using the Feulgen reaction
on 5μ thin parafin sections of spleen. It was observed that Secondary immunized mice showed a lower percentage of apoptosis
as compared to Primary or Unimmunized mice that was subjected to either of the chemotherapeutic drugs. It was thus concluded
that Secondary immunization inhibits the process of chemotherapeutic drug induced apoptosis in vivo. 相似文献
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Feng Gao Xin-yang Hu Xiao-jie Xie Qi-yuan Xu Ya-ping Wang Xian-bao Liu Mei-xiang Xiang Yong Sun Jian-an Wang 《Journal of Zhejiang University. Science. B》2010,11(8):608-617
Mesenchymal stem cell(MSC)transplantation has shown a therapeutic potential to repair the ischemic and infracted myocardium,but the effects are limited by the apoptosis and loss of donor cells in host cardiac microenvironment.The aim of this study is to explore the cytoprotection of heat shock protein 90(Hsp90)against hypoxia and serum deprivation-induced apoptosis and the possible mechanisms in rat MSCs.Cell viability was determined by3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)assay.Apoptosis was assessed by Hoechst 33258nuclear staining and flow cytometric analysis with annexin V/PI staining.The gene expression of Toll-like receptor-4(TLR-4)and V-erb-b2 erythroblastic leukemia viral oncogene homolog 2(ErbB2)was detected by real-time polymerase chain reaction(PCR).The protein levels of cleaved caspase-3,Bcl-2,Bcl-xL,Bax,total-ERK,phospho-ERK,totaI-Akt,phospho-Akt,and Hsp90 were detected by Western blot.The production of nitric oxide was measured by spectrophotometric assay.Hsp90 improves MSC viability and protects MSCs against apoptosis induced by serum deprivation and hypoxia.The protective role of Hsp90 not only elevates Bcl-2/Bax and Bcl-xL/Bax expression and attenuates cleaved caspase-3 expression via down-regulating membrane TLR-4 and ErbB2 receptors and then activating their downstream PI3K/Akt and ERK1/2 pathways,but also enhances the paracrine effect of MSCs.These findings demonstrated a novel and effective treatment strategy against MSC apoptosis in cell transplantation. 相似文献
5.
Edaravone protects PC12 cells from ischemic-like injury via attenuating the damage to mitochondria 总被引：6，自引：0，他引：6
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
6.
Objective： Study blood vessel injury and gene expression indicating vascular endothelial cell apoptosis induced by mannitol with and without administration of anti-oxidative vitamins. Methods： Healthy rabbits were randomly divided into four groups. Mannitol was injected into the vein of the rabbit ear in each animal. Pre-treatment prior to mannitol injection was per- formed with normal saline （group B）, vitamin C （group C） and vitamin E （group D）. Blood vessel injury was assessed under electron and light microscopy. In a second experiment, cell culture specimen of human umbilical vein endothelial cells were treated with mannitol. Pre-treatment was done with normal saline （sample B）, vitamin C （sample C） and vitamin E （sample D）. Total RNA was extracted with the original single step procedure, followed by hybridisation and analysis of gene expression. Results： In the animal experiment, serious blood vessel injury was seen in group A and group B. Group D showed light injury only, and normal tissue without pathological changes was seen in group C. Of all 330 apoptosis-related genes analysed in human cell culture specimen, no significant difference was seen after pre-treatment with normal saline, compared with the gene chip without pre-treatment. On the gene chip pre-treated with vitamin C, 45 apoptosis genes were down-regulated and 34 anti-apoptosis genes were up-regulated. Pre-treatment with vitamin E resulted in the down-regulation of 3 apoptosis genes. Conclusion： Vitamin C can protect vascular endothelial cells from mannitol-induced injury. 相似文献
7.
Objective: To explore how arylamine N-acetyltransferases (NATs) is related to cell apoptosis. Methods: NAT activity in apoptotic HepG2 cells was measured using high performance liquid chromatography (HPLC); the apoptosis rate of HepG2 cells acted upon by an NAT inhibitor was measured using flow cytometry. Results: NAT activity was lowered in apoptotic HepG2 cells;apoptosis rate induced by camptothecin (CAM) increased after inhibition of NAT activity in HepG2 cells. Conclusion: NAT can inhibit apoptosis in HepG2 cells. 相似文献
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SCHMITT Estelle PAQUET Claudie BEAUCHEMIN Myriam BERTRAND Richard 《Journal of Zhejiang University. Science. B》2007,(6)
Tissue homeostasis requires a carefully-orchestrated balance between cell proliferation, cellular senescence and cell death. Cells proliferate through a cell cycle that is tightly regulated by cyclin-dependent kinase activities. Cellular senescence is a safeguard program limiting the proliferative competence of cells in living organisms. Apoptosis eliminates unwanted cells by the coordinated activity of gene products that regulate and effect cell death. The intimate link between the cell cycle, cellular senes- cence, apoptosis regulation, cancer development and tumor responses to cancer treatment has become eminently apparent. Extensive research on tumor suppressor genes, oncogenes, the cell cycle and apoptosis regulatory genes has revealed how the DNA damage-sensing and -signaling pathways, referred to as the DNA-damage response network, are tied to cell proliferation, cell-cycle arrest, cellular senescence and apoptosis. DNA-damage responses are complex, involving “sensor” proteins that sense the damage, and transmit signals to “transducer” proteins, which, in turn, convey the signals to numerous “effector” proteins implicated in specific cellular pathways, including DNA repair mechanisms, cell-cycle checkpoints, cellular senescence and apoptosis. The Bcl-2 family of proteins stands among the most crucial regulators of apoptosis and performs vital functions in deciding whether a cell will live or die after cancer chemotherapy and irradiation. In addition, several studies have now revealed that members of the Bcl-2 family also interface with the cell cycle, DNA repair/recombination and cellular senescence, effects that are generally distinct from their function in apoptosis. In this review, we report progress in understanding the molecular networks that regulate cell-cycle checkpoints, cellular senescence and apoptosis after DNA damage, and discuss the influence of some Bcl-2 family members on cell-cycle checkpoint regulation. 相似文献
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以"细胞的衰老与凋亡"为例,通过创设问题情境、设置认知矛盾、小组讨论、社会话题探讨、迁移应用等活动,以知识为载体,传递正确的生命观念、严密的逻辑思维、严谨的科学探究精神、良好的社会责任感,培养学生的核心素养。 相似文献
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Singh PP Chandra A Mahdi F Roy A Sharma P 《Indian journal of clinical biochemistry : IJCB》2010,25(3):225-243
The antioxidants are essential molecules in human system but are not miracle molecules. They are neither performance enhancers
nor can prevent or cure diseases when taken in excess. Their supplemental value is debateable. In fact, many high quality
clinical trials on antioxidant supplement have shown no effect or adverse outcomes ranging from morbidity to all cause mortality.
Several Chochrane Meta-analysis and Markov Model techniques, which are presently best available statistical models to derive
conclusive answers for comparing large number of trials, support these claims. Nevertheless none of these statistical techniques
are flawless. Hence, more efforts are needed to develop perfect statistical model to analyze the pooled data and further double
blind, placebo controlled interventional clinical trials, which are gold standard, should be implicitly conducted to get explicit
answers. Superoxide dismutase (SOD), glutathione peroxidase and catalase are termed as primary antioxidants as these scavenge
superoxide anion and hydrogen peroxide. All these three enzymes are inducible enzymes, thereby inherently meaning that body
increases or decreases their activity as per requirement. Hence there is no need to attempt to manipulate their activity nor
have such efforts been clinically useful. SOD administration has been tried in some conditions especially in cancer and myocardial
infarction but has largely failed, probably because SOD is a large molecule and can not cross cell membrane. The dietary antioxidants,
including nutrient antioxidants are chain breaking antioxidants and in tandem with enzyme antioxidants temper the reactive
oxygen species (ROS) and reactive nitrogen species (RNS) within physiological limits. Since body is able to regulate its own
requirements of enzyme antioxidants, the diet must provide adequate quantity of non-enzymic antioxidants to meet the normal
requirements and provide protection in exigent condition. So far, there is no evidence that human tissues ever experience
the torrent of reactive species and that in chronic conditions with mildly enhanced generation of reactive species, the body
can meet them squarely if antioxidants defense system in tissues is biochemically optimized. We are not yet certain about
optimal levels of antioxidants in tissues. Two ways have been used to assess them: first by dietary intake and second by measuring
plasma levels. Lately determination of plasma/serum level of antioxidants is considered better index for diagnostic and prognostic
purposes. The recommended levels for vitamin A, E and C and beta carotene are 2.2–2.8 μmol/l; 27.5–30 μmol/l; 40–50 μmol/l
and 0.4–0.5 μmol/l, respectively. The requirement and recommended blood levels of other dietary antioxidants are not established.
The resolved issues are (1) essential to scavenge excess of radical species (2) participants in redox homeostasis (3) selective
antioxidants activity against radical species (4) there is no universal antioxidant and 5) therapeutic value in case of deficiency.
The overarching issues are (1) therapeutic value as adjuvant therapy in management of diseases (2) supplemental value in developing
population (3) selective interactivity of antioxidant in different tissues and on different substrates (4) quantitative contribution
in redox balance (5) mechanisms of adverse action on excess supplementation (6) advantages and disadvantages of prooxidant
behavior of antioxidants (7) behavior in cohorts with polymorphic differences (8) interaction and intervention in radiotherapy,
diabetes and diabetic complications and cardiovascular diseases (9) preventive behavior in neurological disorders (10) benefits
of non-nutrient dietary antioxidants (11) markers to assess optimized antioxidants status (12) assessment of benefits of supplementation
in alcoholics and heavy smokers. The unresolved and intriguing issues are (1) many compounds such as vitamin A and many others
possessing both antioxidant and non-antioxidant properties contribute to both the activities in vivo or exclusively only to
non-antioxidant activity and (2) since human tissues do not experience the surge of FR, whether there is any need to develop
stronger synthetic antioxidants. Theoretically such antioxidants may do more harm than good. 相似文献