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Objective To investigate the regulation of Akt signaling pathway involved in apeptosis of Panc-I cells induced by polyphenol ( - )-epigallocatechin-3-gallate. Methods Pane-1 cells were maintained in DMEM with 10% fetal calf serum in a 95% air,5% CO2 atmosphere,then incubated in different concentrations of EGCG (6.3,12.5,25.0,50.0 μmol/L). The growth arrest effect was determined by MTT assay, and apoptosis was detected by agarose gel electrophoresis. The levels of Akt (60×103 ) and Bad (23×103) were determined by Western blot. Results EGCG time and dose dependently repressed the growth of Panc-1 cells and induced apeptosis in Panc-1 cells ( P <0.05 ). The expression of p-Akt (set473) and p-Bad (ser136) was reduced in a dose-dependent way,whereas the pan-Akt and pan-Bad were unchanged (P < 0.05). Conclusion EGCG can induce apoptosis in pancreatic cancer cells in a dose-and time-dependent fashion by attenuating the blocking effects of Akt signaling pathway on Bad proteins. 相似文献
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Objective To investigate the regulation of Akt signaling pathway involved in apeptosis of Panc-I cells induced by polyphenol ( - )-epigallocatechin-3-gallate. Methods Pane-1 cells were maintained in DMEM with 10% fetal calf serum in a 95% air,5% CO2 atmosphere,then incubated in different concentrations of EGCG (6.3,12.5,25.0,50.0 μmol/L). The growth arrest effect was determined by MTT assay, and apoptosis was detected by agarose gel electrophoresis. The levels of Akt (60×103 ) and Bad (23×103) were determined by Western blot. Results EGCG time and dose dependently repressed the growth of Panc-1 cells and induced apeptosis in Panc-1 cells ( P <0.05 ). The expression of p-Akt (set473) and p-Bad (ser136) was reduced in a dose-dependent way,whereas the pan-Akt and pan-Bad were unchanged (P < 0.05). Conclusion EGCG can induce apoptosis in pancreatic cancer cells in a dose-and time-dependent fashion by attenuating the blocking effects of Akt signaling pathway on Bad proteins. 相似文献
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目的:研究常见影响因素对薄片法血小板聚集实验(SPAT)时间的影响.方法:测定下列富含血小板血浆(PRP)的SPAT:①调整血小板计数分别为240,120,60,30和15×109/L的8例健康献血者PRP;②分别在40,35,30,25,20,15,10和5℃条件下恒温30 min的10例健康献血者PRP;③含终浓度为0,10,20,30,40和50g/L的二甲基亚砜(DMSO)并室温放置30 min的10例健康献血者PRP;④在室温放置1,2,3,4 h后的8例健康志愿者服用阿司匹林前后PRP;⑤含浓度分别为0,0.5,1.0,2.0和3.O U/L的肝素或0.1 g/LEDTA的8例健康献血者PRP.结果:①随着血小板计数的降低,SPAT时间逐渐延长;同一供者血小板计数与其SPAT时间呈显著的直线负相关(r=0.996,P=0.004);②温度在20~40℃对SPAT时间无明显影响,但当温度低于20℃时SPAT时间明显延长;③DMSO对SPAT有明显的影响,使SPAT时间明显延长,并呈明显的剂量效应;④血小板标本室温放置1,2,3和4 h SPAT无显著差异(P=0.815);⑤肝素对SPAT时间无明显影响,而0.1 g/L乙二胺四乙酸(EDTA)可完全抑制血小板聚集.结论:血小板计数、所处的温度以及含有DMSO时,均能在一定程度上影响SPAT时间,但是上述因素均不影响血小板最终形成肉眼可见的聚集,且聚集时间仍然在180 s以内. 相似文献
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背景:氧化应激能够诱导晶状体上皮细胞发生凋亡。
目的:观察Fas蛋白与过氧化氢诱发白内障中晶状体上皮细胞凋亡的关系以及表没石子儿茶素没食子酸酯对Fas蛋白表达及晶状体上皮细胞凋亡的影响。
方法:将健康成年兔透明晶状体随机分为3组:空白对照组仅加入DMEM培养液,过氧化氢组加入DMEM+过氧化氢,表没石子儿茶素没食子酸酯组加入DMEM+过氧化氢+表没石子儿茶素没食子酸酯。
结果与结论:各组体外培养72 h后过氧化氢组晶状体上皮细胞凋亡率及Fas蛋白阳性表达率显著高于空白对照组(P < 0.05)。表没石子儿茶素没食子酸酯组晶状体上皮细胞凋亡率及Fas蛋白阳性表达率显著低于过氧化氢组(P < 0.05)。结果显示,过氧化氢可能是通过上调Fas蛋白的表达诱导晶状体上皮细胞凋亡,而抗氧化剂表没石子儿茶素没食子酸酯可下调Fas蛋白的表达而减轻晶状体上皮细胞的凋亡。 相似文献
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